High Yield Internal Medicine Review for Step 2 CK & Shelf Exam

0:00[Music]

0:05okay what's up guys today we're gonna

0:08cover internal medicine for your shelf

0:10exam or for your step 2 CK so before we

0:14start I just wanted to give some

0:16pointers on when you're doing your

0:19multiple choice questions my first tip

0:21is rule out the other answers my second

0:24tip is if you know one of the answers to

0:26be true and are unsure then pick the one

0:29you know to be true the third tip is if

0:32you don't know pick the more common

0:34things the fourth tip is keep it simple

0:36the fifth tip is if you don't know move

0:39one quick and then try to save time so

0:42you can get the other ones right my

0:44sixth tip is that age is important my

0:46seventh tip is put the whole picture

0:49together and my final tip is when it

0:51comes down to two answers try to reject

0:54one of them

0:56first we're gonna cover criterias so

0:59make sure you know Chad Vasc this is the

1:01score that you apply for atrial

1:03fibrillation CHF hypertension age

1:07greater than 75 counts as two diabetes

1:10stroke counts as two vascular disease

1:14and such as like peripheral artery

1:17disease or coronary artery disease next

1:19is age and then the last one is sex

1:21category as in female so if you have a

1:24score of two or more you want to treat

1:27with warfarin it fits less than that as

1:30in zero or one then you treat with

1:32aspirin so next is Center criteria for

1:36strep pharyngitis so C stands for no

1:39coffee stands for exudates M stands for

1:43nodes as an anterior cervical lymph

1:45nodes t sat stands for temperature if

1:48they're febrile o is four or so if it's

1:52less than 14 years old then you add one

1:55if it's greater than forty four years

1:57old then you minus one point if it's

2:00four plus then you treat empirically

2:04with penicillin and it fits two to three

2:08then you want to do a rapid strep the

2:10exception is in kids you still need to

2:12do a rapid strep test no matter what the

2:15next is pounds criteria which is for

2:17migraine headache so P stands for

2:20pulsatile oh it stands for one day

2:23duration U stands for a unilateral and

2:25stands for nausea and D stands for

2:29debilitating there's no score but it's

2:31kind of just like a mnemonic to help you

2:33diagnose migraine headache versus

2:36tension headache versus cluster headache

2:39the next is curb 65 criteria for

2:41pneumonia so C stands for confusion U

2:45stands for uremia R stands for

2:47respiratory rate as in tachypnea B

2:51stands for blood pressure if they're

2:53hypotensive 65 years old if the score is

2:56two or more you want to hospitalized and

2:58treat the pneumonia in patient usually

3:01first-line inpatient pneumonia is a

3:04fluoroquinolone whereas outpatient it

3:06depends if it's atypical or typical

3:09for typical it'll be amoxicillin and a

3:12typical will be as if through my son

3:14then the Nexus S IRS criteria systemic

3:19inflammatory response system this is

3:21kind of a the way to start tracking to

3:25see if an infection is starting to come

3:26on the first is breathing so if their

3:29tech hip neck that counts as one point

3:32temperature if they are febrile or

3:35hypothermic that counts as one next as

3:38WBC is if they have leukocytosis as one

3:41greater than 12 K or leukopenia less

3:44than four K that's also another point

3:46and then um heart rate if they're

3:49tachycardic that counts as one so two or

3:52more is counts as SI RS if there's a

3:57source of infection then that qualifies

4:00as sepsis if there's infection with

4:03evidence of end organ damage or

4:06hypotension then this is called severe

4:09sepsis and then septic shock is if

4:12someone is hypotensive and it's not

4:16responding to fluids then that's called

4:18septic shock

4:19next is lights criteria for pleural

4:22effusion and lights criteria helps you

4:25differentiate from exudate versus

4:28transudate so usually the two things

4:31you're gonna look at or either protein

4:34or LDH and you compare it from the

4:36pleural fluid to serum so if the ratio

4:39is greater than 0.5 for protein then

4:42that is exudative if it's greater than

4:450.6 for LDH then that's also exudative

4:49there's a third one which has LDH is

4:51greater than two-thirds of the upper

4:54limit of serum LDH but in my experience

4:57i find that kind of useless because most

5:01of the time in the questions you'll get

5:03they'll show you the differences between

5:05pleural fluid and serum and and then you

5:08can calculate the ratio quite easily so

5:11again if any of those ratios are higher

5:14than 0.5 or 0.6 and that's exudate your

5:17differentials for x to date would be

5:20like pneumonia

5:21or malignancy whereas if it's transitive

5:25which is a ratio below that then it's

5:28most likely it's like um

5:30CHF right which causes backing up into

5:33the pulmonary veins and pulmonary

5:35capillaries which causes edema or

5:39cirrhosis which means that because of

5:42your cirrhotic you make less albumin

5:44less intravascular oncotic pressure

5:46which causes edema and then the last

5:50most common one would be in a fraud ex

5:53engine where you're urinating out all

5:55the proteins and that decreases

5:57intravascular oncotic pressure as well

6:00next is well as criteria basically if

6:03the score is four or more then you want

6:06to do a CT angio if it's less than four

6:09then you do a d-dimer well as criteria

6:11is for PE next is COPD so a long term

6:16oxygen therapy criteria makes you

6:19remember if the oxygen saturation is

6:22less than 88 then you want the patient

6:25to be on long-term oxygen therapy at

6:27home or if the pao2

6:29is less than 55 and next is Glasgow Coma

6:33Scale if the score is eight or less that

6:36means including eight then you intubate

6:38next is ascites analysis so a score of

6:42250 plus bootrec cells is indicative of

6:46infection aka spontaneous bacterial

6:49peritonitis

6:50so what someone who and it's usually

6:53seen in patients who are cirrhotic and

6:56have chronic ascites

6:58they'll have diffuse abdominal pain and

7:00fever and leukocytosis the next step is

7:04apparent synthesis if it's greater than

7:06250 that's infection the next one I want

7:10to talk about as the sag gradient the

7:12serum ascites albumin gradient so

7:15basically you're measuring the

7:17differences an albumin from the serum

7:19and the ascites and then you're gonna

7:22take the difference between the two

7:24right and the way I remember which one

7:26goes before is it follows in the name so

7:28there are M minus ascites so if the

7:32score is greater than one

7:33one that's portal hypertension the next

7:36is the Timmy score the Timmy score if

7:39it's between zero to two you want to do

7:41a stress test and the Timmy score is

7:44applied for anyone who has unstable

7:47angina or n STEMI and those with STEMI

7:51automatically go to cath lab but those

7:54with unstable angina or NSTEMI are more

7:57difficult to figure out how to manage

7:59them so that's where you applied the

8:02Timmy score and it fits between zero to

8:05death stress test but if it's three or

8:07more then they go to the cath lab

8:12so we're gonna start cardiovascular

8:14disease so people who have stable angina

8:17which means that they have substernal

8:20chest pain that occurs with exercise or

8:24exertion and is alleviated by rest then

8:27this is a sign of stable angina

8:30because it improves with rest people

8:33with this you the next thing you want to

8:36do is a stress test right and there's

8:39three types of stress tests an EKG an

8:42echo or a nuclear perfusion study so you

8:46would do an echo if that or a nuclear

8:49perfusion study if that person is uh has

8:54any abnormalities on EKG

8:58so the echo so a positive stress test

9:02would be anything that shows ST

9:04depression or hypotension or pain and

9:08then you know the echo you might see

9:11abnormal wall motion that would be a

9:12positive stress test or and then nuclear

9:15perfusion studies would show decreased

9:18uptake of nuclear ice so to open that be

9:20a positive stress test as well so and

9:23then remember if they are unable to

9:26exercise then that's when you do a

9:29pharmacologic stress test so there's two

9:31ways to induce stress on the heart

9:33either

9:34exercise or using drugs such as

9:37adenosine or dye period at a mall so

9:40most of the time the correct answer will

9:43be as exercise stress test using EKG if

9:47they have an abnormal EKG which will

9:50mask the results of the stress EKG then

9:55you either do an echo or nuclear

9:58perfusion studies if they can exercise

10:01then they will exercise on the treadmill

10:04if they can't exercise as an they are

10:07wheelchair-bound or have osteoporosis or

10:10some other thing that is a

10:12contraindication to exercise then that's

10:16when you do a pharmacologic test test

10:19and with the pharmacologic test it can

10:22be observed either on EK

10:25echo or nuclear perfusion study as well

10:28so and then remember that the definitive

10:31way to actually diagnose coronary artery

10:35disease is through angiography so the

10:38reason why you do these stress tests

10:40first is because angiography is very

10:42invasive so that's why you do the others

10:45first so um the first thing you want to

10:48do first test you want to do with chest

10:50pain as EKG the first-line treatment for

10:54stable angina is nitrates aspirin and

10:57beta blockers first-line treatment for

11:00unstable angina is lemonis II - mnemonic

11:04which is morphine oxygen nitrates

11:08aspirin clopidogrel beta blockers ACE

11:11inhibitors statin and heparin and

11:15remember that the first thing you want

11:17to give is aspirin and remember if the

11:21person has unstable angina which means

11:24the definition of unstable angina means

11:27that their angina is worsening or

11:30evolving or occurs at rest now which is

11:34different than stable angina but

11:36unstable angina also has no troponin

11:39elevations if you have unstable angina

11:43with troponin elevations and so

11:47basically unstable angina becomes NSTEMI

11:51as soon as there are any troponin if

11:54there are opponents with st elevations

11:57then this is what we call a STEMI what

11:59alright so when someone comes in with

12:02chest pain the first thing you want to

12:04do is rule out acute coronary syndrome

12:08acute coronary syndrome is unstable

12:11angina and STEMI or STEMI so those are

12:15the three types of acute coronary

12:17syndrome so when someone comes in with

12:19chest pain you want to roll that out so

12:22we first you do an EKG and cardiac

12:25enzymes but the thing is cardiac enzymes

12:28can take a while to come in so first

12:32thing you want to do is what the EKG is

12:34look to see if this

12:36a STEMI or not so if it's Tammy

12:40if it's Tammy then to diagnose Tammy you

12:43don't even need cardiac enzymes all you

12:46need is one millimeter st elevations and

12:49two continuous leads or a new left

12:52bundle branch block with chest pain and

12:55that's considered STEMI you don't even

12:57need the enzymes if you see those they

13:00go straight to cath lab and then see you

13:03do the EKG but there are no st

13:06elevations but they do have the

13:08characteristic chest pain that they were

13:10describing then you wanna do serial

13:14troponin and serial EKGs to see if this

13:17is evolving or changing so then it's

13:20either going to be unstable angina or n

13:23STEMI if the troponin is come back

13:26updated with elevated troponin then

13:29that's now called

13:30an N STEMI as a non ST elevation mi

13:34if there are no opponents yet and after

13:39serial troponin measurements and it

13:41stays low then this is called unstable

13:44angina

13:44and remember if the conditions also have

13:47to be satisfied where the chest pain has

13:50been evolving recently and been getting

13:52worse and this person has been having

13:54chest pain at rest this is called

13:57unstable angina if they have unstable

14:00angina or and STEMI then you want to

14:03apply the Tammy score if it's zero to

14:06two this person will get a stress test

14:08if it's three or more than this person

14:11will go to cath lab anyone who has chest

14:15pain who has has unstable vitals as well

14:18that you suspect my they also go

14:20straight to cath lab so those are some

14:22exceptions main indications for a

14:25cabbage are three vessel disease or

14:28proximal left anterior descending

14:30disease with 70% plus stenosis

14:33next is prinzmetal angina which is

14:36basically coronary vasospasm

14:38so the angiography will show this so

14:41spasm when given or gone a vine or

14:43acetyl choline and you'll also see St

14:46elevation on EKG

14:48during these painful episodes and you

14:50want to treat this with calcium channel

14:52blockers or nitrates you only do TPA and

14:56MMI if there's no access to PCI Center

15:00inferior mi when you have an arrow

15:03cardial infarction of the inferior wall

15:06which is 2/3 and AVF and this is the

15:10only mi that has an exception where you

15:13don't want to give nitrates because

15:15because they have a right ventricular mi

15:19it's already the heart is already having

15:21problems pumping blood to the left side

15:24of the heart so if you give nitrates

15:27this will exacerbate the hypotension

15:29so actually in an inferior wall mi you

15:34actually want to give fluids sometimes

15:37an inferior wall mi can because because

15:41the right coronary artery supplies blood

15:44to the SA node this can cause and then

15:48that sinus bradycardia can cause

15:50cardiogenic shock and usually first men

15:53for cardiogenic shock is dobutamine

15:56which is the beta 1 agonist but in the

16:00case of inferior wall mi that has

16:04bradycardia and cardiogenic shock this

16:07is due to injury of the SA node so in

16:11this special case you want to give

16:13atropine remember that there's only

16:15three drugs shown to decrease mortality

16:17in MI and this is very high yield is

16:20aspirin beta blockers and ACE inhibitors

16:23and nitrates work in two ways but the

16:27predominant way it works by for mi is is

16:30that it decreases preload it's a V no

16:33dilator and that decreases stress on the

16:36myocardium due to excess blood so when

16:39you minimize the preload there's less

16:41stress on the heart muscle and also its

16:45secondary effect as it dilates the

16:47coronary arteries so treatment of

16:49first-degree and second-degree heart

16:52block mobitz one is no treatment but

16:56mobitz ii and the complete heart block

16:58you want to treat with pacemaker drast

17:01Larssen

17:02is an autoimmune pericarditis that

17:05happens two weeks later after an mi host

17:08MI two weeks with fever and symptoms of

17:10pericarditis with leukocytosis you want

17:13to treat it with aspirin this is

17:15contrasted with other causes of

17:17pericarditis such as viral pericarditis

17:19those will be treated with NSAIDs this

17:22dressler syndrome is specifically

17:24treated with aspirin and then you have

17:26restrictive cardiomyopathy I just

17:29remember the OCS

17:30so hemochromatosis amyloidosis

17:34sarcoidosis this creates a diastolic

17:38heart failure with reduced ejection

17:41fraction this is due to deposits in the

17:45myocardium so like amyloid deposits or

17:48granulomas or iron deposits in the

17:52myocardium what I'm trying to say is

17:54remember that hemochromatosis

17:57amyloidosis and sarcoidosis

17:59or if associated with restrictive

18:01cardiomyopathy and then remember

18:04hemochromatosis is bronze diabetes and

18:07iron overload so they'll have diabetes

18:10bronze skimming don't have elevated

18:13liver enzymes amyloidosis is think of

18:17like protein deposits you're gonna have

18:20deposits in the heart and the kidney and

18:22in the joints and in the kidney you'll

18:25see proteinuria versus sarcoidosis is

18:28where you'll see heart and lung stuff so

18:32bilateral hilar adenopathy a dry cough

18:36uveitis erythema nodosum

18:39and also restrictive cardiomyopathy

18:41there are three CHF drugs shown to

18:44decrease mortality and that's ace

18:47inhibitors beta blockers and

18:49spironolactone which is a potassium

18:51sparing they're diuretic which should be

18:54contrasted with the three drugs that

18:57decrease mortality and MI which is ace

19:00inhibitors as well and beta blockers as

19:03well but the third is aspirin remember

19:06metformin which is a first-line

19:08treatment for type 2 diabetes remember

19:11its contraindications we

19:13it's contraindicated in renal disease

19:15and CHF because it can cause metabolic

19:19acidosis remember for CHF acute

19:23decompensation of CHF which means the

19:27heart failure is getting worse then you

19:30want to treat it with them mnemonic no

19:32lit nitrates oxygen loop diuretics

19:36inotropes and positioning such as

19:39elevating the head of the bed but the

19:41first thing you want to treat what is a

19:43loop diuretic such as furiosa might you

19:46need to know

19:47supraventricular tachycardia versus

19:49ventricular tachycardia so a

19:51supraventricular tachycardia will have

19:54narrow qrs s you know it'll look like

19:56QRS TQ r st qrst

19:59and if they're stable you treat with

20:02adenosine and if they're unstable then

20:05you want to treat with cardioversion and

20:08then ventricular tachycardia which has

20:12wide bizarre qrs complexes after one

20:15after another then you want to treat

20:17with amiodarone and if they're unstable

20:20then you want to treat with

20:22cardioversion versus v-fib and pulseless

20:26v-tach first-line treatment for that is

20:29different relation vs asystole and

20:33pulseless electrical activity pulseless

20:36electrical activity means that the EKG

20:39shows any rhythm but when you feel for

20:42the pulse there's no pulse that means

20:44pe-8 and then to treat with that is cpr

20:48and by the way remember that the

20:51first-line treatment for a super

20:53ventricular tachycardia before you

20:56progress with an edema seen is vagal

20:59maneuvers such as carotid massage so

21:02torsades de pointes can lead to v-fib

21:05and this is treated with IV magnesium

21:09which stabilizes the cardiac membranes X

21:12is constrictive pericarditis which is

21:15idiopathic fibrous scarring replacing

21:18the entire pericardial space the key

21:20here I want you to look for is when they

21:23do imaging like

21:25chest x-ray of the heart you'll see

21:27calcifications calcifications is key and

21:30it's usually caused by TB or lupus and

21:33it can present similarly to restrictive

21:36cardiomyopathy it can have equal

21:39diastolic pressures and all chambers and

21:42it can also have by atrial enlargement

21:44and treatment is peri cardiac t'me cute

21:49pericarditis causes the main causes

21:51coxsackievirus and you treat it with the

21:54NSAID verses Jess lair which is treated

21:57with the aspirin aspirin is a type of

21:59NSAID but remember Dressler's aspirin

22:01and on EKG you'll see diffuse St

22:05elevations and it's improved with

22:07leaning forward so cardiac tamponade is

22:11just remember Beck's triad which is

22:14hypotension jvd and muffled heart sounds

22:17it's also associated with pulsus

22:20paradoxus which means when you inspire

22:23this increases filling to the right

22:26ventricle which causes the

22:28interventricular septum to bow over to

22:31the left side which decreases the left

22:34ventricular preload and because of this

22:38the stroke volume is decreased and

22:40because of this the systolic pressure

22:43will drop by greater than 10 and that's

22:46called pulsus paradoxus which means a

22:49systolic pressure dropping by greater

22:53than 10 upon inspiration you will see

22:56that in cardiac tamponade it's also

22:58associated with electric alternans which

23:01means the cure s voltages kind of the

23:05amplitude kind of becomes alternating

23:08between big and small big and small big

23:10and small and that's because the heart

23:13is literally swinging within the

23:16pericardial fluid which distorts the QRS

23:20measurement and then you'll also see

23:23low-voltage QRS and a KU small sine

23:27Kuzma sign which means when you inhale

23:30that the jugular venous distention

23:34increases because with cardiac tamponade

23:37filling of the

23:39right side of the heart is more

23:40difficult because it's not as compliant

23:42so then the venous blood tends to

23:46overflow faster

23:47remember mitral stenosis the majority of

23:50the causes of mitral stenosis our

23:52previous episode of acute rheumatic

23:55fever or rheumatic heart disease

23:57hypertension or aortic stenosis can over

24:01time lead to left ventricular

24:02hypertrophy and if this is prolonged

24:05this can become dilated cardiomyopathy

24:08and people with hypertension or aortic

24:11stenosis tend to get angina because of

24:15decreased perfusion to the coronary

24:17arteries another complication as syncope

24:20due to decreased perfusion of the brain

24:22another complication is left ventricular

24:25hypertrophy because of increased after

24:28load another complication is dilated

24:31cardiomyopathy from chronicity and then

24:35you'll hear a soft s2 because the valve

24:38doesn't move well and then definitive

24:41diagnosis for aortic stenosis is cardiac

24:46catheter to measure the valve area but

24:48an echocardiogram can also measure the

24:51valve diameter if it's less than one

24:54square centimeter or if they have any

24:57symptoms at all such as an angina

25:00syncope or CHF then you want to treat

25:04with valve replacement the tricuspid

25:06valve remember that it's associated with

25:09IV drug use and carcinoid syndrome

25:12carcinoid syndrome is a tumor that

25:15produces too much serotonin and that

25:19creates bronchospasm flushing diarrhea

25:21and right-sided heart murmurs three

25:24causes of holosystolic murmur or mitral

25:27regurg tricuspid regurge and VSD so if

25:32someone has infective endocarditis the

25:35easiest way to diagnose this is someone

25:37who has a fever with leukocytosis and

25:42new onset of murmur and you don't know

25:45the bugs it before you find out from

25:48your blood culture which is the first

25:50thing you want to do you treat it

25:52impaired

25:53with vancomycin and an aminoglycoside

25:56hypertensive emergency is defined as 180

25:59over 120 and the first-line treatments

26:02for hypertensive emergency is IV

26:05hydralazine nitroprusside or labetalol

26:09and remember that for it to be

26:12considered an emergency there has to be

26:15evidence of end organ damage

26:18so encephalopathy or acute kidney injury

26:21or liver injury where versus

26:24hypertensive urgency is high blood

26:28pressure over 180 over 120 but no end

26:33organ damage so the difference is if

26:36it's an emergency you treat IV but if

26:38it's urgency you treat with oral

26:40medications subarachnoid hemorrhage the

26:42Thunder Clap headache worst headache of

26:45your life first thing you want to do is

26:47a CT head without contrast and if that's

26:51negative and you still suspect oh so

26:54brackenreid hemorrhage the next step is

26:56lumbar puncture and you're gonna look

26:58for positive xantho chromia which is the

27:01presence of bilirubin in the CSF a or

27:04DIC dissection is substernal chest pain

27:07that is described as tearing and

27:10radiates to the back and you have two

27:13types type A and type B type B is

27:16anything just go to the left subclavian

27:18and type a is anything proximal to that

27:22and you treat them differently a goes to

27:25surgery right away and B you give beta

27:28blockers to treat it and you diagnose an

27:31aortic dissection with a CT angio or a

27:35transesophageal echo and remember any

27:39type of CT imaging make sure to always

27:42check the patient's kidneys because

27:45anyone with kidney disease it's

27:47contraindicated to use CT with contrast

27:51which is the majority of CT imaging next

27:56is peripheral vascular disease or

27:58peripheral artery disease and so the

28:02number one risk factor is smoking and to

28:05diagnose it you

28:06do something called the ankle brachial

28:08index which is measuring the differences

28:10in blood pressures from the ankle and

28:13the arm and if the ratio in the ankle to

28:17arm is less than 0.9 then that's disease

28:20and if it's less than 0.4 then this is

28:23severe disease which will most likely

28:25have pain at rest as well and people

28:30with peripheral artery disease will

28:31describe themselves as having

28:33claudication in their legs while walking

28:37so they'll walk a certain distance and

28:38then feel pain in their legs and then it

28:41improves with rest it's sort of like

28:43stable angina of the legs due to

28:47stenosis of the ephemeral or popliteal

28:50arteries the ones that are current rest

28:52would be synonymous to like unstable

28:55angina and then sometimes they can make

28:57clots which is called acute limb

29:00ischaemia which would be synonymous to

29:03like an MI so if someone has a ratio

29:07between 0.4 to 0.9 which would be like

29:10stable angina this is the initial stages

29:13of peripheral vascular disease the

29:16first-line treatment is an exercise

29:18program if it starts if they start to

29:20have problems at rest and their ratio is

29:23below point 4 now you have to do an

29:25intervention such as a stent or a bypass

29:29if if they have acute limb ischaemia

29:32which is due to some sort of thrombosis

29:35that cuts off the circulation in the

29:38legs where everything just still did

29:40that starts getting cold and pulseless

29:42and in a lot of pain then you want to

29:45treat that with heparin or an

29:49embolectomy sometimes there's a

29:51variation of peripheral vascular disease

29:54known as LaRouche syndrome which is

29:57caused by atherosclerosis proximal to

30:00the aortic bifurcation before they

30:03become the iliac arteries and this

30:06person will complain of bilateral leg

30:10pain as well as the key here is

30:12impotence and buttock pain and this is

30:16us like a sub type of there

30:18creation of the same thing remember that

30:21IVC filters are placed

30:23if contraindicated to heparin or

30:26warfarin or if they've failed previous

30:29therapy with heparin or warfarin if you

30:31suspect a PE in a patient which is

30:34basically acute side and onset of

30:37tachypnea tachycardia and hypoxemia the

30:41first thing you want to do is give

30:44heparin before you even do the CT angio

30:47so heparin and then CT angio if you had

30:51to pick what is the best next step and

30:53they all so those are the options pick

30:56heparin first and then low molecular

30:59weight heparins remember they're

31:01contraindicated in renal disease someone

31:05who has venous insufficiency looked for

31:08the medial malleolus ulcer which is a

31:11sign of venous insufficiency which can

31:14be contrasted to other similar

31:17presentations such as CHF cardiogenic

31:20shock first-line treatment is the ina

31:23trope such as dobutamine septic shock

31:25first-line treatment is IV antibiotics

31:29plus IV fluids and potentially based

31:32oppressors neurogenic shock remember

31:35everything is down cardiac output is

31:37down heart rate is down total peripheral

31:40resistance is down wedge pressure is

31:43down and the jvd is down and you treat

31:46this with IV fluids

31:50so now we're gonna do pulmonology so

31:52COPD is chronic obstructive pulmonary

31:56disease which is seen in chronic smokers

31:58and sometimes alpha 1-antitrypsin

32:01deficiency COPD has two different

32:05variations one is chronic bronchitis and

32:08the other is emphysema so chronic

32:11bronchitis has excess mucus production

32:13from mucous glands hypertrophy and thus

32:16narrows the airways

32:18whereas emphysema is where you have

32:20destruction of the alveoli so on on

32:23auscultation of the lungs

32:25you will hear hyper resonance on

32:27percussion because why because the

32:29alveoli are all destroyed so this

32:32increases the amount of air in the lungs

32:34you have decreased breath sounds because

32:37it's an obstructive lung disease so it's

32:39harder for them to exhale you'll also

32:41hear crackles why because people with

32:44chronic bronchitis will have excess

32:47mucus production and that will produce

32:50crackles also in the alveoli that are

32:53blown out they will also have access to

32:57mucus in there which causes crackles and

32:59then wheezes is due to airway narrowing

33:02from the mucus and land hypertrophy so

33:06only two things decrease mortality in

33:08COPD and that's quitting smoking and

33:11home oxygen and then COPD the stages are

33:15based on fev1 percentage so greater than

33:1880% is mild moderate is 5280 severe is

33:223250 and very severe is less than 30 and

33:26depending on each stage you have

33:28different types of treatments so for 80

33:31and above it's albuterol for 50 to 80

33:34you want to add a petroleum from 30 to

33:3750 you want to add an inhaled steroid

33:40and for less than 30 that's when you add

33:43long-term oxygen so remember there are

33:47two other indications for adding home

33:49oxygen and that's a pao2 of less than 55

33:54or an oxygen saturation of less than 88

33:57and then people who have Co

33:59the exacerbation the key I want you to

34:02look for here is anyone with COPD who

34:05has an change in sputum production

34:08whether it's increased bunam or a change

34:11in color that's a an exacerbation you

34:15want to do a chest x-ray to rule out

34:17possible pneumonia but if it's an

34:20exacerbation you add IV steroids and an

34:24antibiotic such as fluoroquinolone or as

34:28a throw Meissen and you also give

34:31non-invasive positive pressure

34:33ventilation but you don't want to exceed

34:3693% because this can cause shunting COPD

34:42with pneumonia

34:43this is treated with zosyn or cefepime

34:47zosyn is also known as piperacillin and

34:50Tazo back to them but the thing is I

34:52want you to remember a COPD patient with

34:55pneumonia

34:56the most common bug is Pseudomonas

34:59asthma patient with normal this is this

35:03is high-yield it's a question where a

35:05patient who's coming with an acute

35:08exacerbation of asthma and they're in

35:10respiratory distress but they're pco2 as

35:13normal or elevated what should you do

35:15next intubate why because a patient with

35:19asthma should be hyperventilating so

35:22they should have respiratory alkalosis

35:24so their co2 should actually be low if

35:27it's normal that means that they're

35:29getting tired and they're not able to

35:31blow all the pco2 so respiratory failure

35:35is basically inevitable so you want to

35:39intubate before that happens so asthma

35:41there's also four stages that you need

35:44to know so there's intermittent piled

35:46persistent moderate persistent and

35:48severe persistent so mild intermittent

35:52is like less than twice a week mild

35:54persistent is three to seven days a week

35:58moderate persistent is every day and

36:00severe persistent as multiple times a

36:03day so at each stage you want to add a

36:05different drug so at mild intermittent

36:08which is less than twice a week you can

36:10just do albuterol Piron

36:12but then as it progresses you want to

36:15add a low steroid and the next stage you

36:18want to add a medium steroid and then

36:20the final stage you want to add a high

36:22dose installed steroid you can also have

36:24a Q X asthma exacerbation and in this

36:28one you want to first give albuterol but

36:31you want to also give IV a roid and

36:34oxygen whereas in COPD exacerbation you

36:39also give IV steroids and oxygen but you

36:43also add antibiotics bronchiectasis is

36:46permanent dilatation of the bronchi and

36:48loss of cilia caused by recurrent

36:52infections and what this will cause is a

36:54lot of mucus and so this person will be

36:57coughing out buckets and buckets of

36:59mucus every day and cystic fibrosis is

37:02the most common cause this is a form of

37:05obstructive lung disease because of the

37:08blown out bronchi and you diagnosis with

37:11the high-resolution CT and you treat it

37:14with bronchodilators exacerbations are

37:17treated with antibiotics

37:19cystic fibrosis this is autosomal

37:22recessive all secretions are thick

37:24because the chloride transport channel

37:27doesn't work and water will follow it so

37:29all the secretions are very thick

37:31remember the ages so less than 20 is

37:35associated with staph aureus

37:38but above 20 is associated with

37:40Pseudomonas in terms of pneumonia and

37:43you treat this with supplementing things

37:45such as pancreatic enzymes vitamins DEA

37:48k supplementation and inhaled darkness

37:51which helps break down the secretions

37:54and the lungs so next I want to talk

37:56about can cause tumors so Pancoast tumor

37:59x' is a lung cancer in the upper lobe of

38:02the lung and this can cause different

38:05manifestations and complications so it

38:07can cause Horner syndrome

38:09superior vena cava syndrome phrenic

38:12nerve palsy recurrent laryngeal nerve

38:15palsy remember superior vena cava

38:17syndrome is if you have some sort of

38:19obstruction that impairs the drainage of

38:22the veins into the SVC so a long

38:25turmeric

38:26do that I know it present with edema of

38:29the face and arms and then Horner

38:31syndrome is if you have invasion of the

38:33sympathetic ganglion and then this would

38:36give you ptosis miosis anhidrosis

38:38sometimes the tumor can invade the

38:41brachial plexus which causes weakness

38:44and the right arm you can have phrenic

38:47nerve palsy as well which causes one

38:51diaphragm to be higher than the other

38:53and then recurrent laryngeal nerve palsy

38:56which causes voice hoarseness so those

38:59are the complications and remember that

39:01smokers tend to have central lung tumors

39:05and the most common ones are squamous

39:07cell carcinoma or small cell carcinoma

39:10and remember that the squamous cell

39:13carcinoma produces PTH RP parathyroid

39:17hormone-related peptide so that can

39:20cause hypercalcemia and hypophosphatemia

39:23with a low PTH because it's the PTH RP

39:28that's causing the hypercalcemia and

39:30then small cell cancers are associated

39:33with SIADH ACTH secretion and

39:38lambert-eaton which is when you have the

39:41antibodies presynaptic calcium channel

39:44receptor which prevents the release of

39:47acetylcholine at the neuromuscular

39:49Junction versus myasthenia gravis

39:52lambert-eaton will improve with usage

39:54whereas myasthenia gravis has weakness

39:57that worsens with usage adenocarcinoma

40:00is associated with non-smokers and

40:03they're more on the peripheries the next

40:06point is really high yield if you have a

40:07vignette where a patient has a nodule on

40:10chest x-ray a new nodule what is the

40:13best next step the best next step is to

40:16find a previous chest x-ray to compare

40:19if it changed then you want to do a CT

40:23after that if you don't have any old

40:27imaging in the vignette like tough

40:30compared to then the next step is CT so

40:33signs of pneumothorax would be one-sided

40:36decreased breath sounds hi

40:39resonance and decreased fremitus

40:41fremitus is the vibration from palpation

40:44and then versus tension pneumothorax the

40:48key here is the tracheal deviation and

40:51tension pneumothorax will also have

40:53hypotension because of compression of

40:56the IPC ya and then remember they're

40:58treated differently so just a normal new

41:01more sera thorax you can treat with a

41:03chest tube whereas tension pneumothorax

41:06you have to do a needle

41:07thoracentesis first because it's quicker

41:10this is more urgent right here to

41:13release the air and then you can take

41:16your time and put in the chest tube

41:18afterwards interstitial lung disease the

41:21ABCs of interstitial lung disease are

41:24asbestosis beryllium cold

41:27silicosis and sarcoidosis and on chest

41:30x-ray you will see reticular nodular

41:33ground glass appearances or honeycomb a

41:36asbestosis is also associated with

41:39pleural plaques and mesothelioma and

41:42then silicosis has the eggs shell

41:45calcifications of their upper lobes

41:48speaking of upper lobes there's three

41:51things that like to go for the upper

41:52lobes and it's silicosis TB and

41:56Aspergillus sarcoidosis can also produce

42:00interstitial lung disease and remember

42:02earlier I saying that it can cause

42:04restrictive cardiomyopathy

42:06but for sarcoidosis remember on chest

42:09x-ray you'll see the bilateral hilar

42:12adenopathy and this in sarcoidosis all

42:15the vignettes look at the calcium

42:17they'll always have hypercalcemia

42:19because the granulomas tend to make more

42:22calcium and then ACE enzyme is also

42:25elevated and you treat this with

42:27steroids

42:28so for respiratory failure people who

42:30have low pao2 think of lung diseases and

42:33people who have a high pco2 think of

42:37hypoventilation and that means they have

42:40difficulty getting air out so think of

42:43like obesity hyperventilation or COPD

42:47whereas a low po2 think of like

42:50interstitial lung disease

42:52next you need to know about the basics

42:54of mechanical ventilation so there are

42:58four parameters and so there are there's

43:00title volume and respiratory rate and

43:03there's fio2 and peep and each one of

43:06them either helps manipulate pco2

43:10or pao2 so in terms of pco2 this is for

43:15ventilation

43:16so tidal volume and respiratory rate

43:18will help alter your PC o2 levels if you

43:22increase tidal volume then you can

43:25exhale your pco2 more so increasing

43:28tidal volume will lower the pco2 more an

43:32increasing respiratory rate will also

43:35lower pco2 and vice versa and then pao2

43:40is as an analogue of oxygenation so you

43:46can control that with fio2 and peep the

43:49higher the fio2 the higher the PA o -

43:53the higher the peep the higher the PA o

43:55- and vice versa and you'll get a

43:58question where someone's on mechanical

44:01ventilation and their pco2

44:03might be too high out of the normal

44:06range and they'll ask you what should

44:08you change and then look for either

44:10increasing tidal volume or respiratory

44:13rate usually the tidal volume is a

44:16better answer than respiratory rate

44:19because it can change the pco2 more

44:22efficiently a RDS is caused by some sort

44:27of systemic infection like

44:29pyelonephritis or like severe

44:31pancreatitis and this is where you have

44:34increased vasodilation of the pulmonary

44:37capillaries which causes leakage into

44:40the alveoli and then collapsing of the

44:43alveoli and you want to treat this with

44:46high peep and low tidal volume so

44:48remember high peak pulmonary

44:51hypertension is diagnosed with pulmonary

44:53artery pressure greater than 25 and this

44:57is just something you have to memorize

44:58because a lot of times in the questions

45:00some of the things you'd need to just

45:02memorize because they're not in the lab

45:05so another thing that you might want to

45:07memorize is like lactate is normal is

45:10less than 1 over 1 is considered lactic

45:15acidosis aspiration pneumonia this is

45:18caused by people who are on mechanical

45:20ventilation or people who have impaired

45:23gag reflexes such as those with dementia

45:27or seizures or alcoholics or stroke

45:31patients and you want it first and they

45:34don't cause um right lower lobe

45:37pneumonias or abscesses and you want to

45:39treat this with an antibiotic that

45:41covers anaerobes

45:43and that's clindamycin Pneumocystis

45:45euroace is an opportunistic infection

45:48and patients with AIDS or if those who

45:51are immunosuppressed from transplant

45:54Oregon transplant and you prophylaxis

45:58with TMP SMX and this is the kicker is

46:02you gotta remember when do you give

46:04steroids in a Pneumocystis your

46:06eventually infection and you give

46:09steroids

46:09if the pao2 is less than 70 or the AAA

46:13gradient is greater than 35 and remember

46:16in AIDS patients you start giving

46:19prophylaxis 40mp SMX at a cd4 less than

46:23200 and also know how it presents which

46:27is basically like the atypical pneumonia

46:29which is fever non-productive cough with

46:33bilateral interstitial infiltrates

46:38we're gonna talk about GI so staging of

46:41colon cancer is done with CT so most

46:45cancers after you diagnose it they'll

46:48ask you what's the next thing to do and

46:51always think about staging with CT max

46:53so whether it's colon cancer ovarian

46:57cancer lung cancer best next step after

47:01diagnosis is a CT diverticulosis is

47:05diagnosed with a barium enema it causes

47:08a lot of blood in the toilet bowl and

47:11then diverticulitis diagnosed with a CT

47:14scan with contrast acute mesenteric

47:17ischemia is diagnosed with angiography

47:21and remember this is the one where it's

47:24basically an MI of the mesenteric

47:27arteries it's due to emboli or

47:30thrombosis and da the key here is pain

47:33out of proportion the patient will have

47:35extreme abdominal pain but the physical

47:39abdominal exam will be unimpressive no

47:41peritonitis no guarding nor rigidity

47:44very mild tenderness to palpation and

47:46usually multiple risk factors for

47:50atherosclerosis or do vascular disease

47:53like hypertension hyperlipidemia

47:55diabetes smoking that's kind of the

47:58vignette for acute mesenteric ischemia

48:00also associated with afib because afib

48:04is gonna build up those thrombi that

48:07will embolize to mesenteric arteries

48:10Ogilvie syndrome is just think of like

48:13Elias of the colon it's isolated so on

48:17abdominal x-ray you'll see it descended

48:19just standed colon but the small

48:21intestines look okay this is usually an

48:24older person post off another post-op

48:27kind of presentation that's similar to

48:29this is post-op paralytic ileus but the

48:33difference here is that the small bowel

48:36and the colon we'll both be distended

48:39and the key here is that Anna Elias

48:41there will be decreased bowel sounds

48:43sigmoid volvulus is treated with the

48:46sigmoidoscopy and then on abdominal

48:50x-ray that's where you'll see the omec

48:52Meg

48:53or lick the bean sign when you put the

48:55scope up it it will help detours the

48:58volvulus remember for varices

49:02secondary to cirrhosis first-line meds

49:05or octreotide and then for prophylaxis

49:09is a beta blocker because our trio tide

49:13is actually a splanchnic vessel facial

49:17constrictor and that prevents blood from

49:20reaching the venous side and by doing

49:23that it helps alleviate the amount of

49:26blood in the portal system in the veins

49:30next is spontaneous bacterial

49:33peritonitis I already talked about this

49:36but anyone with cirrhosis with chronic

49:38ascites who developed a fever and

49:41diffuse abdominal pain think of

49:44spontaneous bacterial peritonitis you

49:47diagnose it with a paracentesis which

49:50shows lots of neutrophils greater than

49:52250 and that's diagnostic and you treat

49:55that with ceftriaxone remember a young

49:58girl who takes an oath oral

50:00contraceptive pill who has a new mass on

50:03the liver the diagnosis is a hepatic

50:06adenomas so this is a highly associated

50:10with a young girl taking an O CP and you

50:14only resect it if it's greater than 5

50:17centimeters next as delivery abscesses

50:21and cysts so you have a hydatid liver

50:23cysts which is caused by a kind of

50:26caucus and this is associated with

50:28people from Latin America who have had

50:32close contacts with dogs those are your

50:34buzz words and you treat it with

50:36resection and my been dissolve on right

50:39upper quadrant ultrasound you will see a

50:42round shape with a lot of other small

50:46cysts within it many many multiple cysts

50:50within cysts and then a pyogenic liver

50:53abscess is a complication of ascending

50:56cholangitis so and then ascending

50:59cholangitis is a complication of co-lead

51:03o caliph Isis so with

51:06and so if you have inflammation and

51:08infection of the common bile duct this

51:11can ascend up to the liver and cause a

51:14pyogenic liver abscess the most common

51:17causes ecoli you diagnose it with the

51:20ultrasound or CT and to treat it you do

51:24an IND plus antibiotics

51:27remember with this one if you leave it

51:29alone it can be fatal

51:31the last is amoeba liver abscess such a

51:34caused by entamoeba histolytica and um

51:39this just the buzz words are fever right

51:43upper quadrant pain plus diarrhea and so

51:47the other liver cysts won't really have

51:50diarrhea which makes the amoebic liver

51:53abscess stand out and you treat this

51:57with metronidazole so also in the

52:00amoebic liver abscess the patient will

52:02also have yo sin Ophelia because this is

52:05a parasite and remember parasites will

52:08cause elevations in Yosef is physiologic

52:11jaundice of the newborn this is due to

52:14an immature conjugating system and this

52:17is caused and this causes a indirect

52:22hyperbilirubinemia which is the same as

52:25unconjugated hyperbilirubinemia and this

52:28will happen after a few days of life

52:31remember that if a baby has a newborn

52:36has jaundice right at birth this is

52:39pathologic and the next best step is a

52:42Coombs test

52:43Craig learn ajar is due to a deficiency

52:46of glue coronal transferees and that

52:50causes a unconjugated hyperbilirubinemia

52:53and think of gilbert disease as like

52:56craig learn ajar light like it this

52:59person has a deficiency not a complete

53:02deficiency of glue coronal transferees

53:05it's only apparent when they have when

53:08they're sick

53:08so the vignette will be like a 20 year

53:10old guy who recently had some sort of

53:13infection and now he has jaundice that

53:15is unconjugated hyperbole

53:18anemia this is Gil bears syndrome and

53:21then there's Dubin Johnson which is

53:24where the how parasites are able to

53:27conjugate bilirubin but they can't

53:29release it so the patient will have a

53:31black lever and then rotor is basically

53:35juban johnson light which is the same

53:38mechanism but they will have a normal

53:42colored

53:43liver and then the mnemonic for causes

53:46of elevated ast and alt or ABCDE F G H I

53:52so autoimmune hepatitis B hepatitis C

53:56drugs ethanol fatty liver growths like

54:00tumors hemodynamic instability like

54:04hypotension which can lead to shock

54:06liver and iron such as iron overload

54:09semen hemochromatosis

54:10if you suspect cholecystitis what's the

54:13best next step right upper quadrant

54:16ultrasound if it's equivocal which means

54:19they have all the signs of cholecystitis

54:21right upper quadrant pain fever

54:24leukocytosis a positive Murphy sign and

54:27then you do the right upper quadrant

54:29ultrasound but there's no gallbladder

54:31wall thickening no Perico Lee cystic

54:33fluid no gallstones president what's the

54:36next step is a HIDA scan the hiatus scan

54:39is a diet which lights up the entire

54:41biliary tree and if the gallbladder

54:44doesn't light up that means that there's

54:46a stone there blocking it and that will

54:48help you diagnose cholecystitis so HIDA

54:51scan is used if the right upper quadrant

54:54ultrasound is non diagnostic and to

54:58diagnose cholecystitis

55:00you need two of the three on right upper

55:03quadrant ultrasound which is what I said

55:06earlier

55:07Perico logistic fluid Bal bladder wall

55:10thickening which means greater than four

55:11millimeters and gall stones present

55:14again co-lead vocalist Isis is the

55:17president of the stone lodged in the

55:20common bile duct if this is there long

55:22enough this can cause an infection such

55:24as ascending cholangitis and ascending

55:27cholangitis is classified with the triad

55:30of Charcot is triad what

55:32right upper quadrant pain fever and

55:35jaundice and this can be expanded

55:37further to something called Reynolds

55:40pentad which adds altered Mental Status

55:42plus hypotension

55:44so cholangitis ascending cholangitis

55:47remember the main cause is ecoli and if

55:50that ascends further up that can cause a

55:52pyogenic liver abscess but before that

55:56complication happens if you can't catch

55:58ascending cholangitis you're gonna treat

56:01it with IV fluids IV antibiotics and one

56:05type of intervention what is it it's

56:08gonna be an ERCP

56:09you do go through endoscopic retrograde

56:13cholangiopancreatography and retrieve

56:16that stone another complication of kali

56:19Dhokla with Isis is that it can go down

56:22and obstruct the pancreatic duct it can

56:25do that but a lot of times you won't

56:27find it but this will cause something

56:29called gallstone pancreatitis and then

56:32so this is a classic board question as

56:35well is someone who has been diagnosed

56:38with pancreatitis through elevated

56:41lipase amylase and with the clinical

56:43signs and symptoms of pancreatitis and

56:45the diagnosis is clear what's the best

56:48next step in terms of imaging CT abdomen

56:53or Rea upper quadrant ultrasound the

56:56answer will be right upper quadrant

56:58ultrasound because the amylase and

57:00lipase are already elevated you don't

57:02need a CT to diagnose pancreatitis so

57:06the best next imaging is finding the

57:08source and the most common source is

57:11gall stones and the second most common

57:15is alcohol so if you find gall stones

57:19you found your called Brit the next

57:21thing you need to know is that this

57:23patient needs a cholecystectomy within

57:26the same hospital visit because it's

57:29just gonna happen again and so you might

57:32as well eliminate the source one other

57:35final complication of cholecystitis is

57:39that sometimes the stone can erode

57:42through the gall bladder and

57:45through adjacent small intestine and

57:48this can go all the way down to the

57:51terminal ileum and cause a blockage

57:52there and that's called call stone le s

57:55so a person will have the presence of

57:59air in the gallbladder wall and this is

58:03called gallstone le s and the patient

58:05will present with symptoms of small

58:07bowel obstruction so they'll have a

58:10distension proximal to the le s possible

58:13small air fluid levels and also

58:16hyperactive bowel sounds with nausea and

58:21Billy s vomiting and obstinance

58:24constipation plus not passing gas and

58:27diffuse abdominal pain so that is the

58:31last complication of cholecystitis

58:33actually just kidding there's one more

58:35complication of cholecystitis which is

58:37in the ICU patient this is a classic

58:40question as well an ICU patient can

58:43actually get predisposed to something

58:46called a calculous cholecystitis

58:48which means um the ICU patient is

58:52usually on TPN alot and that means that

58:55their gallbladder is under active it

58:57doesn't contract a lot and this can

58:59predispose to bacterial colonization the

59:03second one is to prolonged ischemia

59:06which causes ischemia of the gall

59:08bladder and this will cause a calculous

59:11cholecystitis and then the right upper

59:14quadrant ultrasound will show no stones

59:16but everything else is indicating that

59:19there's a cholecystitis and they'll ask

59:21you how do you treat it and you treat a

59:24calculous cholecystitis

59:25with percutaneous Coley's estas to me so

59:29that means you put your draining putting

59:32a tube through the skin and through the

59:34gall bladder and your draining it

59:36through the skin remember primary

59:38sclerosing cholangitis which is when you

59:41get the beaded appearance of the biliary

59:43tree this is highly associated with

59:45ulcerative colitis they always like to

59:48ask this a patient with ulcerative

59:50colitis has an association with primary

59:54sclerosing cholangitis

59:55and then primary biliary cirrhosis

59:58which is also known as primary biliary

1:00:01cholangitis it's autoimmune remember it

1:00:05has the anti mitochondrial antibodies

1:00:07and the key here is that they have

1:00:10extreme pruritus you want to treat this

1:00:14with earth so dial appendicitis

1:00:17remember is diagnosed clinically you

1:00:21sometimes they might ask you what's the

1:00:23best next step and it'll say a

1:00:25appendectomy B CT of the abdomen and

1:00:28this can be tricky but you only do a CT

1:00:32if the diagnosis of appendicitis isn't

1:00:36clear-cut so maybe they'll have right

1:00:38left lower quadrant pain but like a

1:00:40negative wrong saying or like a negative

1:00:43so assign or no rebound tenderness but

1:00:46it seems so much like it that's when you

1:00:49would do a CT but if they have all the

1:00:51positive signs of appendicitis like

1:00:53nausea vomiting right lower quadrant

1:00:56pain that started Perry umbilical it's

1:00:58at McBurney's point there's a positive

1:01:01Robson sign positive rebound tenderness

1:01:03positive psoas sign they have zero

1:01:06appetite then and fever leukocytosis the

1:01:11diagnosis is clear-cut the answer will

1:01:14be appendectomy but if any of those kind

1:01:17of are contradicted then pick CT scan

1:01:19and this one requires a little bit of

1:01:22finesse but just that's kind of the

1:01:24point they're trying to get at is that

1:01:26appendicitis is able to be diagnosed

1:01:30clinically carcinoid tumor secretes

1:01:32serotonin it's most commonly found in

1:01:35the appendix and the small bowel

1:01:37remember that these people are prone to

1:01:40niacin deficiency because if you

1:01:42remember tryptophan makes serotonin

1:01:45melatonin and niacin and if you have a

1:01:48lot of serotonin due to carcinoid a

1:01:51carcinoid tumor then this will hog up

1:01:54all the tryptophan and then the person

1:01:57will be left with no niacin and

1:01:59melatonin and then niacin which is

1:02:01vitamin b3 has the three DS remember

1:02:04diarrhea dermatitis and dementia and

1:02:07carcinoid tumors have the B FDR

1:02:11mnemonic bronchospasm flushing diarrhea

1:02:13and right-sided heart valve

1:02:16abnormalities pancreatic pseudocyst is a

1:02:19common complication of pancreatitis it's

1:02:22a cyst that appears two to three weeks

1:02:25after acute pancreatitis and usually the

1:02:29person will have early satiety a

1:02:31distended abdomen and like big abdominal

1:02:34pain and then imaging will show assess

1:02:37and then the answer is usually observe

1:02:40but if it's really big like five

1:02:42centimeters or greater than you drain it

1:02:45and then chronic pancreatitis I just

1:02:48want you to remember the word

1:02:50calcification so chronic pancreatitis

1:02:52will help calcifications and then this

1:02:55is a common common complication of

1:02:58aortic surgery that I want you to

1:03:00remember is a a Ordo enteric fistula

1:03:03which is from after a or the surgery the

1:03:07patient's a aorta can actually kind of

1:03:11like the gallstone ileus mechanism a

1:03:13hole can erode through the aorta into

1:03:16the intestines and then so you'll have a

1:03:19lot of bleeding from the aorta crossing

1:03:21over into the GI system so this patient

1:03:24will have bright red blood per rectum

1:03:26and a recent a or deque surgery and this

1:03:30is a Ordo enteric fistula achalasia

1:03:34is failure of the lure esophageal

1:03:37sphincter to relax remember that the

1:03:39mechanism is failure to relax and then

1:03:43any patient who has problems swallowing

1:03:46such as dysphasia remember the

1:03:50first-line imaging is a barium swallow

1:03:53so the differentials could be sankar x'

1:03:56it could be an esophageal cancer it

1:03:59could be esophageal spasm

1:04:01it could be crass syndrome and it could

1:04:05be esophageal stricture the list is

1:04:08endless but any time someone has

1:04:10problems swallowing the first step is

1:04:14barium swallow unless they have alarm

1:04:18symptoms and alarm symptoms would be

1:04:20anyone who is greater than 55 years old

1:04:24with problem swallowing and weight loss

1:04:28remember as anchors diverticulum the

1:04:31vignette will be an old man who has a

1:04:34difficulty when they eat they feel like

1:04:37they get food stuck in the back of their

1:04:39throat and and it doesn't go all the way

1:04:41down and also don't have the buzzword

1:04:45here's halitosis really smelly breath

1:04:47remember that GERD can predispose to

1:04:51esophageal stricture and this can cause

1:04:55difficulty with swallowing foods and

1:04:58liquids most common cause of peptic

1:05:01ulcer disease which basically means

1:05:03gastric or duodenal ulcers is H pylori

1:05:07or NSAID use remember anyone who comes

1:05:11in with gastritis symptoms of heartburn

1:05:14symptoms of GERD if they're young and

1:05:18from North America the first-line

1:05:21treatment is proton pump inhibitor

1:05:24therapy and to come back in a few weeks

1:05:26to see if that helps if they're from

1:05:29another country where H pylori is very

1:05:32prevalent like Asia for example then the

1:05:36first thing you want to do is offer h

1:05:38pylori testing through the urease breath

1:05:41test or the h pylori fecal antigen

1:05:45testing but if anyone has symptoms of

1:05:49heartburn GERD gastritis but have alarm

1:05:54symptoms then the next best step this is

1:05:56high yield is endoscopy so alarm

1:06:00symptoms would be microcytic anemia

1:06:03weight loss or elderly age so 55 years

1:06:08or older if someone comes in with

1:06:10symptoms of heartburn and they are 55

1:06:13years or older then the next best step

1:06:16is endoscopy the next thing to is anyone

1:06:20who is older than 50 years old who has

1:06:24microcytic anemia due to iron deficiency

1:06:28anemia this is colon cancer until proven

1:06:31otherwise so the next best step very

1:06:34classic question

1:06:36is a colonoscopy and remember you do a

1:06:39colonoscopy when people turned 50 years

1:06:43old and you do it every 10 years and

1:06:45unless they had a family member who had

1:06:49colon cancer before the age of 60 then

1:06:52you want to do this at 40 years old or

1:06:5510 years before the relative was

1:06:59diagnosed with cancer whatever one comes

1:07:02first

1:07:02inflammatory bowel disease has is either

1:07:06Crohn's disease or ulcerative colitis

1:07:08and remember Crohn's disease has skipped

1:07:11lesions it can also include the oral

1:07:14mucosa like oral ulcers and it's

1:07:17associated with structure and fistulas

1:07:20whereas ulcerative colitis always

1:07:23includes the rectum and this is only

1:07:26mucosal whereas cones is transmural and

1:07:29then this one is happens in like giant

1:07:33strips and is continuous and then

1:07:37remember that ulcerative colitis is

1:07:39associated with primary sclerosing

1:07:41cholangitis and inflammatory bowel

1:07:44disease is treated with sulfasalazine

1:07:47and in acute flares it's treated with

1:07:50steroids and inflammatory bowel disease

1:07:54has a high-yield cutaneous Association

1:07:57which is pyoderma gangrenosum this is

1:08:01associate with IBD and pyoderma

1:08:03gangrenosum is a sterile wound and it's

1:08:07treated with steroids not antibiotics

1:08:10because it's sterile is treated with

1:08:11steroids and that is gastroenterology

1:08:16all right now we're gonna talk about

1:08:17endocrine so remember with the first

1:08:23thing you want to do with a thought new

1:08:26thyroid nodule is TSH and ultrasound so

1:08:30TSH helps determine whether the nodule

1:08:33is hyper thyroid or a youth thyroid

1:08:35hyper thyroid nodules are usually not

1:08:38malignant whereas youth thyroid nodules

1:08:41tend to be well most malignant nodules

1:08:45are you thyroid the ultrasound hat gives

1:08:49you visual information information

1:08:51whether it's cystic if it's multi

1:08:53loculated which is could be a sign of

1:08:55cancer or the size whether it's greater

1:08:58than a centimeter or less than a

1:09:00centimeter so it's important to know the

1:09:02diagnostic algorithm so basically if the

1:09:05person is has a hyper thyroid nodule the

1:09:08next best step is radioactive iodine

1:09:11uptake and this will help tell whether

1:09:14it's diffuse or one nodule or

1:09:18multinodular so if it's diffuse that's

1:09:21Graves disease if it's one area then

1:09:23that's toxic adenoma just one area if

1:09:26it's patchy and multiple then that's a

1:09:29multi nodular toxic goiter which is also

1:09:33known as Plummer disease if they are you

1:09:36thyroid then the next thing you want to

1:09:38do is if they are if it's greater than a

1:09:40centimetre then you biopsy if it's less

1:09:43than a centimetre then you wait and

1:09:45follow-up in a few weeks because less

1:09:48than a centimetre has a low likelihood

1:09:50of malignancy

1:09:51so another thing too is sometimes a

1:09:55patient can be hyper thyroid with zero

1:10:00radioactive iodine uptake what's

1:10:02happening there so basically radioactive

1:10:06iodine uptake is an indicator of how

1:10:09much thyroid hormone is actually being

1:10:12made it's like a thyroid Factory so if

1:10:14there's uptake you know that that

1:10:16thyroid gland is taking up the iodine

1:10:19and making more sometimes it you can be

1:10:23hyper thyroid and have no uptake so what

1:10:26does that mean no act take me

1:10:28not actively making thyroid and

1:10:32basically think of like a bursted gland

1:10:35or an inflamed gland so classic examples

1:10:38of hyper thyroid with no uptake would be

1:10:42like a postpartum thyroiditis or dick or

1:10:46vein disease which is also known as sub

1:10:49acute thyroiditis or you can think of

1:10:53Hashimoto's thyroiditis which can have a

1:10:56hyper thyroid phase so what that means

1:10:59is that there's they're not actively

1:11:01making thyroid but the thyroid gland is

1:11:04leaking out preformed thyroid so it's

1:11:07basically like a like a dam that has

1:11:10broken open and so all that preformed

1:11:13thyroid hormone is out in the

1:11:15circulation but that factory is broken

1:11:18they're they're not making any more new

1:11:21thyroid so when you see someone who's

1:11:23hyper thyroid with no uptake think of

1:11:26the diseases that cause inflammation of

1:11:30the thyroid that would cause it to leak

1:11:33out so next is when you have excess

1:11:36estrogen whether it's through

1:11:38medications or a pregnancy this

1:11:41increases the thyroid binding globulin

1:11:43and because this increases then it kind

1:11:47of attaches to all the thyroid hormone

1:11:50and that the thyroid hormone under a

1:11:54healthy normal person will make more

1:11:57thyroid hormone to keep up with the new

1:12:00tbg being made but people who are

1:12:03hypothyroid already can't make enough

1:12:07thyroid so when they are pregnant or

1:12:10taking OCPs the tbg will increase but

1:12:13their thyroid won't be able to keep up

1:12:16with all that new tbg which is binding

1:12:19up all the thyroid hormone so then they

1:12:21become even more thyroid deficient so my

1:12:24point is that people who are pregnant or

1:12:28on OCPs who are hypothyroid need to

1:12:31increase their levothyroxine dosages to

1:12:34keep up with the increased TBG so anyone

1:12:39who's pregnant or taking OCPs

1:12:41who is

1:12:42needs to take more levothyroxine than

1:12:46their usual dose Hashimoto's is also

1:12:49known as chronic lymphocytic thyroiditis

1:12:51and this is associated with other

1:12:56autoimmune diseases such as lupus or

1:12:59pernicious anemia or shrug ins disease

1:13:02remember as a general rule anyone who

1:13:05has autoimmune disease is automatically

1:13:08more prone to getting other autoimmune

1:13:11diseases and the key higher yield thing

1:13:14i want you to know with Hashimoto's is

1:13:16that it's associated with thyroid

1:13:19lymphoma so subacute

1:13:21de Quervain thyroiditis is remember the

1:13:25key here is they're hyper thyroid but

1:13:28out of all of the hyperthyroidism the

1:13:31buzzword here is painful so a hyper

1:13:34thyroid patient with the painful thyroid

1:13:37who recently had an upper respiratory

1:13:39tract infection

1:13:40this is subacute de Quervain thyroiditis

1:13:42and remember this is caused by leakage

1:13:47of excess tyroid hormone so think back

1:13:50to when I was talking about radioactive

1:13:53uptake this will have decreased uptake

1:13:55and you treat this with NSAIDs or

1:13:58aspirin and then the last is medullary

1:14:01thyroid cancer

1:14:03remember this arises from the para

1:14:05follicular C cells which make calcitonin

1:14:08calcitonin helps bring calcium levels

1:14:11back down whereas parathyroid hormone is

1:14:15made by the parathyroid gland which

1:14:18helps increase calcium so they're in

1:14:21different glands that oppose each other

1:14:23so that can be confusing so make sure

1:14:25you review your Anatomy if that's fuzzy

1:14:28but Manjula tyroid cancer I want you to

1:14:31remember that a lot of times when this

1:14:34is diagnosed the treatment is surgery

1:14:38but before you treat with surgery you

1:14:42have to remember that Maj Larry thyroid

1:14:44cancer is part of the men to a and men2b

1:14:49diseases and remember men to a is

1:14:53ppm and men2b

1:14:57is p mm so pheochromocytoma parrot

1:15:02hyperparathyroidism and imaginary

1:15:05thyroid cancer and meant to be is

1:15:08pheochromocytoma medullary thyroid

1:15:11cancer and mucosal neuromas or marfanoid

1:15:15habitus and so as soon as you think of

1:15:18medullary thyroid cancer you have to

1:15:20remember Oh men - amen to be and because

1:15:24of that the next best step is to assess

1:15:28for those other diseases why the most

1:15:32important one you want to check for is

1:15:34pheochromocytoma so if they say this

1:15:37person was diagnosed with medullary

1:15:39thyroid cancer what's the best next step

1:15:42a thyroidectomy be urine matter urine

1:15:47madam nephrons C de etc the answer is

1:15:51urine meta nephrons why because you

1:15:54gotta assess that they have

1:15:55pheochromocytoma why because if you

1:15:58don't and you do I read surgery what if

1:16:01they have an episode of pheochromocytoma

1:16:03where they're they get a hypertensive

1:16:06emergency and just bleed out and die so

1:16:09that's why it's really important to make

1:16:11sure that they don't have

1:16:12pheochromocytoma so again to diagnose

1:16:16pheochromocytoma it's urine meta

1:16:18nephrons that's one of the classic board

1:16:20questions they asked with modular

1:16:22thyroid cancer to see if you know what

1:16:26are the men to a and meant to be

1:16:27diseases and then on top of that what

1:16:30kind of blood tests would you order to

1:16:33be able to diagnose pheochromocytoma so

1:16:36there's multiple layers to that and

1:16:38that's why it's a classic board question

1:16:40so acromegaly is caused by excess growth

1:16:44hormone in the pituitary and remember

1:16:47that the first test is it a growth

1:16:50hormone or B igf-1 the answer is igf-1

1:16:54which is released by the lever which is

1:16:57stimulated by growth hormone this is

1:16:59more reliable than growth hormone

1:17:02because the levels are

1:17:03assistant lee hye-in acromegaly versus

1:17:07growth hormone which the levels can

1:17:09fluctuate the first-line treatment for

1:17:11SI da da CH is water restriction so

1:17:15anyone you suspect with Cushing syndrome

1:17:18remember there's a mnemonic BAM

1:17:20cushingoid Buffalo Hump amenorrhea moon

1:17:24crazy ulcers skin changes hypertension

1:17:28infection necrosis of the femoral head

1:17:31glaucoma osteoporosis immunosuppression

1:17:36and diabetes the first test is an

1:17:39overnight dexamethasone suppression test

1:17:42a 24-hour cortisol level or a late night

1:17:46salivary cortisol level for a dreama

1:17:49insufficiency the first test will be

1:17:51urine cortisol or ACTH stimulation if

1:17:54the ACTH stimulation test boosts up the

1:17:59cortisol levels then you know that this

1:18:02is a secondary adrenal insufficiency

1:18:04caused by the pituitary gland whereas if

1:18:07it doesn't go up then you know this is a

1:18:09primary adrenal insufficiency which is

1:18:12an adrenal problem and that's called

1:18:14Addison's disease and Addison's disease

1:18:17the most common cause is autoimmune so

1:18:20the next is if a patient has

1:18:22hypertension with hypernatremia and

1:18:25hypokalemia then the first step you want

1:18:29to do is a random 2 aldosterone ratio so

1:18:33why is that because you want to

1:18:35determine if the cause of this

1:18:38hyperaldosteronism is adrenal problem or

1:18:42if it's due to a under perfusion of the

1:18:45kidneys problem mainly mainly renal

1:18:48artery stenosis or fibromuscular

1:18:50dysplasia so if the aldosterone is high

1:18:53in the randomness' low then this

1:18:55suggests an adrenal problem which is

1:18:58called constant room whereas if the

1:19:01ranan is high and then the aldosterone

1:19:03is high this suggests a renal artery

1:19:06stenosis or fibromuscular dysplasia

1:19:09because stenosis of the renal artery

1:19:12will cause decreased perfusion to the

1:19:16Jade

1:19:16sells and then the jg sells will

1:19:19increase Renan and remember the wrasse

1:19:22system Renan will convert

1:19:25angiotensinogen to angiotensin one and

1:19:28then ace angiotensin converting enzyme

1:19:32will convert angiotensin 1 to

1:19:34angiotensin 2 and then angiotensin 2

1:19:38goes all the way to the adrenal cortex

1:19:40remember there's three layers the zona

1:19:43glomerulosa the zona fascicle RS and the

1:19:47zona reticularis and then salt sugar sex

1:19:50so aldosterone in the outermost layer

1:19:54cortisol in the metal layer and sex

1:19:57hormones in the innermost layer the

1:19:59medulla underneath that is where

1:20:01catecholamines released that's where

1:20:03fewer chromosome happens but the

1:20:06angiotensin 2 will go to zona

1:20:09glomerulosa and then increase the

1:20:12synthesis of aldosterone aldosterone

1:20:15will then go all the way to the

1:20:18principal cells the principal cells

1:20:21remember aldosterone is a steroid

1:20:24hormone so steroid hormones work

1:20:26intracellularly it'll go inside the cell

1:20:30and bind the aldosterone

1:20:32mineralocorticoid receptors and this

1:20:34will increase transcription and

1:20:37translation of the emac channel and then

1:20:40that will help draw in sodium and the

1:20:44potassium channel will excrete potassium

1:20:47and that with drip bringing in sodium

1:20:50water will follow so this person will

1:20:52have hypernatremia hypokalemia and with

1:20:56the increased water will lead to

1:20:58hypertension so that's why with people

1:21:02with hypertension hypernatremia and

1:21:05hypokalemia the first thing you want to

1:21:07do is a random tell dosterone ratio to

1:21:10help narrow your differential remember

1:21:12the classic patient with renal artery

1:21:15stenosis is an older person with the

1:21:17history of hypertension that's been well

1:21:20controlled and now all of a sudden

1:21:22they've they've been adherent to their

1:21:25medications now all of a sudden their

1:21:27blood pressures

1:21:28control and multiple medications aren't

1:21:31helping and it's being bit refractory to

1:21:35treatment you should think of renal

1:21:37artery stenosis in addition to that on

1:21:40abdominal auscultation there will be a

1:21:42murmur over the renal artery whereas

1:21:45fibromuscular dysplasia the the

1:21:47stereotypical

1:21:49classic patient will be a young female

1:21:51who has a bruit over the renal arteries

1:21:55with unexplained hypertension with like

1:21:58I said again hypernatremia hypokalemia

1:22:01and also in fibromuscular dysplasia its

1:22:05associated with the sub auricular breed

1:22:08a bruit by the ears so diabetes mellitus

1:22:12is diagnosed with three ways either to

1:22:15fasting readings of greater than 126

1:22:18random glucose level of 200 with

1:22:21symptoms such as polyphagia polydipsia

1:22:24polyuria dehydration weight loss or a

1:22:27humid loeben a1c of 6.5 Plus remember

1:22:31metformin is contraindicated in CHF and

1:22:37kidney failure because it can exacerbate

1:22:39lactic acidosis metformin is

1:22:42contraindicated when creatinine levels

1:22:45are greater than 1.5 sometimes they like

1:22:48to ask you what are the effects of

1:22:50metformin and the three big ones are

1:22:52enhances insulin sensitivity it blocks

1:22:55gluconeogenesis and it decreases GI

1:22:58absorption metformin is also the

1:23:01first-line treatment of type 2 diabetes

1:23:03the most common cause of death in a

1:23:06diabetic patient is myocardial

1:23:09infarction due to accelerated

1:23:11atherosclerosis it's also on a side note

1:23:15the most common cause of death in

1:23:17rheumatoid arthritis is also myocardial

1:23:20infarction due to the same mechanism so

1:23:23you should know the difference between

1:23:25hyperglycemic hyperosmolar state vs. DKA

1:23:29and the main kicker is the pH so a

1:23:32person with DKA will have anion

1:23:35metabolic acidosis whereas the person

1:23:38with HHS won't and the glucose levels

1:23:41are very different to a person with HHS

1:23:44will have glucose levels of near 1000

1:23:46whereas a person with DKA has glucose

1:23:49levels of around 3 to 500 so those are

1:23:52the two main differences and then

1:23:54remember dk8 you're gonna have anion gap

1:23:58metabolic acidosis right so a pH of less

1:24:01than seven point three five right and

1:24:04then the anion gap will be sodium minus

1:24:08chloride minus bicarb which will be

1:24:10greater than the sources always change

1:24:14sometimes it's 8 to 12 sometimes it's 8

1:24:16to 16 I use 8 to 16 anything greater

1:24:19than 16 is the anion gap metabolic

1:24:22acidosis

1:24:24this person usually has a type 1

1:24:26diabetic who's not making any insulin

1:24:29they'll have abdominal pain nausea and

1:24:31vomiting and they'll have respiratory

1:24:34alkalosis to compensate for the

1:24:37metabolic acidosis this is called coos

1:24:39moles breathing deep tachypnea with

1:24:42giant tidal volumes you want to treat

1:24:45this with continuous insulin and IV

1:24:48fluids and you would give potassium if

1:24:51the potassium levels drop below five

1:24:54point two because sometimes they show

1:24:57hyperkalemia but their whole body is

1:25:00actually potassium deficient because of

1:25:03due to the hydrogen potassium exchanger

1:25:05so remember if your acidotic

1:25:08the hydrogen out in the blood will want

1:25:11to go into the cells and this will

1:25:13exchange with potassium and if this

1:25:16keeps happening the intracellular stores

1:25:19of potassium are depleted but the

1:25:21vascular stores of potassium are

1:25:23increased so you want to monitor the

1:25:25potassium and the question here is when

1:25:27do you stop giving insulin and that's

1:25:31when the anion gap has closed where as

1:25:34HHS is treated with IV fluids and

1:25:37insulin as well and then last is

1:25:40zollinger-ellison which is gastrin tumor

1:25:43you'll see that multiple duodenal ulcers

1:25:45with diarrhea and you diagnose that

1:25:48with gastrin levels and not the gastrin

1:25:51levels will be over a thousand and then

1:25:54the next thing you'll do is a secretin

1:25:56challenge and secretin usually lowers

1:25:59gastrin levels but it doesn't lower the

1:26:02gastrin levels in this case and this is

1:26:04a diagnosis of the zollinger-ellison and

1:26:07treatment is proton pump inhibitor or

1:26:09surgery and last is glucagon oma and the

1:26:13key here is hyperglycemia plus a classic

1:26:16rash called necrotizing migratory

1:26:18erythema if you see this rash it's a

1:26:21glucagon OMA and then speaking of

1:26:23glucagon if someone has beta blocker

1:26:26overdose what's the antidote

1:26:28it's the glucagon and that is endocrine

1:26:33next as CTN joint diseases so a fetus

1:26:37with congenital heart block what does

1:26:39that mean it's associated with neonatal

1:26:41lupus so I want you to know the

1:26:45treatment regimens for rheumatoid

1:26:48arthritis and lupus so rheumatoid

1:26:51arthritis for mild so there's they have

1:26:55similar treatments that's why I wanted

1:26:57to compare and contrast them so

1:26:59rheumatoid arthritis mild disease is

1:27:02treated with any sets and then the

1:27:04disease modifying drug of choice is

1:27:08methotrexate and for rheumatoid

1:27:11arthritis flares it's treated with

1:27:13steroids versus lupus the mild version

1:27:18of lupus is treated with NSAIDs

1:27:19the disease modifying is

1:27:22hydroxychloroquine so the disease

1:27:24modifying drugs are different and then

1:27:26for flares is also steroids and you

1:27:29diagnose rheumatoid arthritis based on

1:27:32the clinical presentation of bilateral

1:27:35smidge symmetric metacarpal phalangeal

1:27:38and proximal interphalangeal joint

1:27:41stiffness and erythema that's worse in

1:27:45the morning and it improves throughout

1:27:46the day it spares the di P what you'll

1:27:49do is it'll have elevated ma elevated

1:27:53rheumatoid factor and the specific one

1:27:55is elevated anti citrulline aidid

1:27:58protein anti-ccp and then vs lupus

1:28:03there's a mnemonic soap brain MD Sarah

1:28:06situs so all like they could have

1:28:08pleuritis pericarditis oral ulcers

1:28:11arthritis photosensitivity which means

1:28:15that their skin gets burned really

1:28:18easily and blisters easily blood so

1:28:21pancytopenia anemia thrombocytopenia

1:28:25leukopenia renal they can have lupus

1:28:29nephritis syndrome which is a

1:28:30combination of hematuria and proteinuria

1:28:33a na i is immunoglobulins so that should

1:28:37remind you

1:28:38of anti double-stranded DNA and anti

1:28:42Smith antibodies and then and for Nero

1:28:47there can be psychiatric manifestations

1:28:49of lupus and m4 Matt malar Ashe and d4

1:28:53discoid rash so four out of those eleven

1:28:57means that there's a 99% chance that you

1:29:00have lupus

1:29:00the next is antiphospholipid syndrome

1:29:03this person is the female who has had

1:29:06recurrent miscarriages and random

1:29:09episodes of thrombotic episodes like DVT

1:29:13or PE and it's usually as a prolonged

1:29:16PTT and Pt that isn't corrected by a

1:29:19mixing study and they also have false

1:29:22elevations of VDRL so false if for less

1:29:26positives and remember that this person

1:29:29has a hypercoagulable state so gout is a

1:29:33sudden onset of super painful joint the

1:29:38classic joint is the meta tarsal

1:29:40phalangeal joint the base of the big toe

1:29:43will be inflamed and swollen and it will

1:29:46be super painful with an acute onset

1:29:49that can even wake the patient up at

1:29:51night the next step is arthrocentesis

1:29:54you want to analyze the fluid and in the

1:29:58an Allah in the fluid it'll show

1:30:00negatively birefringence holes which

1:30:04will be yellow needle shaped crystals

1:30:06that will be diagnostic for gout if

1:30:09there are positively birefringence holes

1:30:12rhomboid shaped crystals then this is

1:30:15called pseudo gout and pseudogout is

1:30:18associated with contro calcine OSIS

1:30:20which is where on x-ray you'll see

1:30:23calcifications of cartilage and then GAO

1:30:25that acute flare is treated with NSAIDs

1:30:28or colchicine the contraindication for

1:30:31that is kidney disease so someone with

1:30:34CKD you can't give NSAIDs or colchicine

1:30:37so then the next treatment which would

1:30:40be intra articular steroids the next is

1:30:43knowing the difference between

1:30:45polymyositis versus polymyalgia

1:30:49nikhat vs. fibromyalgia they love to

1:30:52test you on knowing the differences but

1:30:55the key thing here is that polymyalgia

1:30:58rheumatica is think stiffness

1:31:01polymyositis think weakness and

1:31:04fibromyalgia think pain so those are

1:31:07your starting points so let's start with

1:31:09polymyositis so this person has

1:31:11symmetric weakness CPK will be elevated

1:31:16because this is due to inflammation of

1:31:19the muscles so CPK is an a muscle enzyme

1:31:22so this will be elevated and you treat

1:31:25this with steroids polymyositis also can

1:31:29have cutaneous manifestations the two

1:31:32high yields ones are Goren's papules

1:31:34which are red papules over the knuckles

1:31:37and heliotrope rash which is a rash

1:31:40around the orbit of the eye the key

1:31:42thing here too I want you to remember is

1:31:44that polymyositis is usually associated

1:31:47with the underlying malignancy next is

1:31:51polymyalgia rheumatica polymyalgia

1:31:54rheumatica think of an elderly patient

1:31:56with stiffness and pain in their hip and

1:32:01shoulders and usually this person will

1:32:04have an elevated ESR but the CPK will be

1:32:08normal and then you treat this with low

1:32:10dose steroids polymyalgia rheumatica is

1:32:14also associated with something called

1:32:16temporal arteritis or giant cell

1:32:19arteritis which is vasculitis of the

1:32:22temporal artery along the side of the

1:32:25head it will be big and inflamed and

1:32:27this is an emergency because it can

1:32:29cause blindness so you want to treat

1:32:32that well when you biopsy it you'll see

1:32:35giant cells but you want to treat it

1:32:37with high-dose steroids and polymyalgia

1:32:40rheumatica is extremely responsive to

1:32:43storage so they'll see immediate

1:32:44improvement lastest fibromyalgia and I

1:32:47want you to think about pain especially

1:32:50over the trigger points so they have

1:32:52symmetric pain on pressure points over

1:32:55the neck the shoulders the butt the

1:32:58knees all along the back

1:32:59and the pain is considered constant and

1:33:02aching remember that this person there's

1:33:05us is associated with mood disorders and

1:33:08somatic symptom disorder the treatment

1:33:11for this is I their TCA or an SNR I like

1:33:15venlafaxine and then anybody with a

1:33:17sudden onset of psoriasis or people who

1:33:21have molluscum contagiosum remember that

1:33:24this is associated with HIV so the best

1:33:28next step is to test for HIV and that is

1:33:33CT and joint diseases

1:33:38right next is renal so white blood cell

1:33:41casts in your in the two big ones I want

1:33:44you to think about our acute

1:33:46interstitial nephritis and

1:33:47pyelonephritis so uremia so that's from

1:33:52kidney disease where the urea levels are

1:33:55really high it can impair utley lip

1:33:57function so this can cause an increased

1:34:00bleeding time but there are four

1:34:02manifestations of uremia that I want you

1:34:05to remember that are indications for

1:34:07dialysis so one is hemolytic uremic

1:34:10syndrome which is a form of

1:34:12microangiopathic hemolytic anemia

1:34:15remember that this is where you get the

1:34:18platelets clumping and then the red

1:34:20blood cells going by and then they shear

1:34:23which causes thrombocytopenia and a

1:34:26mini-me oh that's H us which can also be

1:34:30precipitated by Antero hemorrhagic you

1:34:34coli heck which is associated with

1:34:37eating undercooked burgers and then and

1:34:41usually people with AK when they're

1:34:43treated with antibiotics leches

1:34:45fluoroquinolones will lead to H us but

1:34:48uremia can also lead to H us the second

1:34:51is uremic pericarditis people have

1:34:54chronic kidney disease with pericarditis

1:34:57that's you riemeck pericarditis platelet

1:35:00dysfunction so they can have elevated

1:35:03bleeding times and if they start

1:35:05bleeding out or confusion which is just

1:35:09called uremia and they would have

1:35:10asterixis with that those are the

1:35:13manifestations of uremia and all of

1:35:15those are treated with dialysis the top

1:35:19two causes of CKD or hypertension and

1:35:22diabetes mellitus so um remember we're

1:35:27gonna talk about other dialysis

1:35:29indications and the mnemonic is a e i o

1:35:32u so acidosis

1:35:34which is refractory electrolytes

1:35:38hyperkalemia that's also refractory

1:35:41intoxications overload as in fluid

1:35:45overload from CKD and uremia

1:35:48symptoms so the intoxications there's a

1:35:51sub mnemonic which is mail which is

1:35:54methanol aspirin lithium and ethylene

1:35:57glycol those for substitute substances

1:36:01when you're intoxicated with them those

1:36:03are also die Eliza Bull so acute

1:36:06interstitial nephritis I want you to

1:36:08remember and said diuretics and

1:36:11antibiotics this is an allergic reaction

1:36:14to medications the mnemonic is fear

1:36:17fever yoson ophelia azo tamiya meaning

1:36:21kidney injury and rash so when I think

1:36:25of a cute interest to show them the

1:36:27Friday's I think of someone who recently

1:36:29took drugs and now they have hematuria

1:36:33with white blood cell casts remember

1:36:36white blood cell casts you'll see in

1:36:38either acute interstitial nephritis or

1:36:40pyelonephritis so when I see white blood

1:36:43cell casts that kind of makes me

1:36:45suspicious right away and then if they

1:36:48have a rash on top of that it's a it's a

1:36:51grand-slam this is a cute interstitial

1:36:53nephritis versus acute tubular necrosis

1:36:55which can be caused by hypoxia or toxins

1:37:00when you are hypoxic or there's under

1:37:03perfusion so the kidney assay that

1:37:06patient went into shock so they had pre

1:37:09renal azo tamiya remember if the buin

1:37:12Preetam ratio is greater than 20 that's

1:37:15pre renal sot mia if there's not enough

1:37:18blood flow reaching the kidneys then the

1:37:22tubules can dry up and necrosis and

1:37:25that's called acute tubular necrosis

1:37:27certain toxins can do this as well but

1:37:30the classic vignette is someone who went

1:37:33into shock and later developed acute

1:37:36kidney injury and so the key here is on

1:37:40microscopic your analysis you will see

1:37:43muddy brown casts and then this is just

1:37:46treated with IV fluids

1:37:48next is the renal tubular acidosis so

1:37:53remember when you have metabolic

1:37:56acidosis the first thing you wanted to

1:37:58is check whether the anion gap is this

1:38:02anion gap metabolic acidosis or not

1:38:05anion gap metabolic acidosis the anion

1:38:08gap

1:38:08everyone knows the mnemonic mud piles

1:38:10methanol uremia DKA propylene glycol

1:38:14isoniazid lactic acidosis ethylene

1:38:18glycol and salicylates but non-ionized

1:38:21gap metabolic acidosis people tend to

1:38:24just um get lost on it but it's so just

1:38:30keep it simple the two most common

1:38:32causes of non anion gap metabolic

1:38:36acidosis are diarrhea because you poop

1:38:40out all the bicarb so that makes you

1:38:42acidotic or the next most common one is

1:38:45the rtas renal tubular acidosis and it's

1:38:49not that hard there's three types you

1:38:51need to know RTA type 1 type 2 and type

1:38:544 so RTA type 1 number 1 should remind

1:38:59you of one letter H H should remind you

1:39:03of hydrogen so type 1 is due to under

1:39:07excretion of hydrogen you lock up all

1:39:10the hydrogen so you get acidotic one

1:39:13should also remind you of stones so

1:39:16kidney stones has the letter you have to

1:39:20spell stone by spelling 1 st o n e so

1:39:25RTA type 1 is associated with kidney

1:39:29stones type 2 2 should remind you by b.i

1:39:33- by that's bicarb you cannot absorb

1:39:38bicarb properly so you lose a lot of

1:39:41bicarb that makes you acidotic type 4

1:39:44four letters should remind you of a LD o

1:39:48l dosterone so this is hypoalle dose

1:39:52grown so hyponatremia hyperkalemia

1:39:56remember with aldosterone it actually

1:40:00people always remember you increase you

1:40:03absorb sodium and excrete potassium but

1:40:06people always forget that aldosterone

1:40:08action also excrete

1:40:10hydrogen as well through the Alpha

1:40:13intercalated cells and so when you lose

1:40:17all that hydrogen you become alkalotic

1:40:19but that's when aldosterone is working

1:40:23but this is hypoalle dosterone ism

1:40:25so all the hydrogen gets kept so that

1:40:29makes you acidotic and the key thing

1:40:32here is that's the only one that has

1:40:34hyperkalemia

1:40:35so with those little kickers that should

1:40:38help you if there's kidney stones

1:40:40non at anion gap metabolic acidosis RTA

1:40:43type 1 if there's a non anion gap

1:40:46metabolic acidosis with hyperkalemia

1:40:49that's type 4 if it's not neither of

1:40:51those probably type 2 and then remember

1:40:54if you have a metabolic alkalosis what's

1:40:58the next best step the next best step is

1:41:01to check the urine chloride why because

1:41:05if the chloride is high right the urine

1:41:08chloride is high that means the kidneys

1:41:10are unable to absorb chloride so this is

1:41:14a kidney problem and if the urine

1:41:16chloride is low then this is most likely

1:41:19another problem a GI problem such as

1:41:23vomiting and you vomit out all the acids

1:41:26so you get alkalotic remember that

1:41:28steatorrhea so fatty stools when it

1:41:31reaches the terminal ileum this can bind

1:41:34up the calcium this is also known as

1:41:36saponification and when it binds up the

1:41:40calcium remember that this is a cool

1:41:43concept because oxalate and calcium tend

1:41:48to bind at the terminal ileum and then

1:41:50that makes it insoluble so you poop it

1:41:53out calcium oxalate but if the fat is

1:41:56stealing all the calcium and binding to

1:41:59it then oxley has nothing to bind to and

1:42:02that's still soluble so it gets

1:42:04reabsorbed and goes to the kidneys

1:42:06instead when it goes to the kidneys it

1:42:09finds another friend it finds calcium in

1:42:12the tubules so that will make calcium

1:42:14oxalate in the kidney tubules become

1:42:17insoluble and make kidney stones

1:42:20so basically

1:42:22we eating high fat foods predisposes to

1:42:25calcium oxalate kidney stones also this

1:42:29is a trick tricky one too as sometimes

1:42:31people ask with calcium oxalate stones

1:42:34do you want to increase calcium uptake

1:42:37or decrease calcium uptake because

1:42:39people think Oh calcium oxalate stones

1:42:42or if you eat a lot of calcium that'll

1:42:44make more calcium oxalate stones that's

1:42:46not true when you eat when you eat a lot

1:42:49of calcium the calcium goes to the

1:42:51terminal ileum same thing it'll bind up

1:42:54all the oxalate and then you'll be able

1:42:57to poop out all the calcium oxalate if

1:42:59you have a low calcium diet then that

1:43:02oxley is free to go back and reabsorb

1:43:05back into the kidneys and make calcium

1:43:07oxalate stones there so basically my

1:43:11point is if someone has kidney stones

1:43:13you want to have a low salt diet a low

1:43:16fat diet and a high calcium diet and

1:43:21also drink a lot of water to make the

1:43:23crystals more soluble an elderly male

1:43:26who smokes a lot who has gross

1:43:29painless hematuria I want you to think

1:43:31about two things either renal cell

1:43:33carcinoma or a bladder cancer renal cell

1:43:36carcinoma the person will also on top of

1:43:40the hematuria will also have a flank

1:43:43pain and abdominal mass if that's true

1:43:46the next thing what you want to do is a

1:43:48CT of the abdomen and then treat it with

1:43:52a nephrectomy but if the person doesn't

1:43:54have an abdominal mass or flank pain

1:43:57then the next thing you should think

1:43:58about is bladder cancer and it's most

1:44:01likely transitional cell carcinoma this

1:44:05is due to the carcinogens and cigarette

1:44:07smoke

1:44:08the carcinogens are trapped in the urine

1:44:10a lot and it tends to pool in the

1:44:13bladder and that can cause cancer and

1:44:15then if you suspect bladder cancer which

1:44:18is gross painless hematuria in a chronic

1:44:23smoker without any signs of renal cell

1:44:26carcinoma so no abdominal mass or flank

1:44:28pain then the next best step is a

1:44:31cystoscopy next is a young male with

1:44:34irregular

1:44:36the shaped testicle a painless mass and

1:44:39the testicle what's the next best step

1:44:42is a scrotal ultrasound you want to see

1:44:45if the if that's actually a mass the

1:44:48mass could be a potential cancer the

1:44:51next step is an inguinal orchiectomy you

1:44:55don't want to biopsy it because of

1:44:57potential seeding of the scrotum so if

1:45:00it's basically diagnosed on ultrasound

1:45:03and then you're just gonna remove it

1:45:05testicular torsion versus epididymitis

1:45:08they like to compare these so remember

1:45:11that testicular torsion is when you get

1:45:13twisting of around the spermatic cord

1:45:16and it cuts off the blood supply this is

1:45:18a cute onset of severe testicular pain

1:45:22but the cord the spermatic cord is

1:45:25non-tender

1:45:26if you elevate the scrotum it's worse

1:45:30with elevation and the key

1:45:32distinguishing factor here is the

1:45:33cremasteric reflex

1:45:35if you stroke the medial aspect of the

1:45:38upper thigh the scrotum more under

1:45:42normal conditions will raise but in this

1:45:44one that reflex is absent

1:45:47whereas in epididymitis it's present

1:45:50another key distinction is epididymitis

1:45:53is an infection so this person will also

1:45:57have fever but their cord will be tender

1:46:00and also upon elevation it's relieved so

1:46:04those are the differences but if I had

1:46:07to remember the key differences

1:46:08epididymitis will have a fever and then

1:46:11a testicular torsion has no cream

1:46:15aesthetic reflex and if you're unsure

1:46:17about the diagnosis of testicular

1:46:19torsion like in the vignette the picture

1:46:23is not very clear and they asked what's

1:46:25the best next step then you want to do a

1:46:28scrotal ultrasound see there might be

1:46:30mixed features um but if it's very clear

1:46:34the diagnosis is clear-cut and there's

1:46:36no contradicting and that's what I mean

1:46:39by clear-cut if all the facts are

1:46:41textbook but if one of the facts kind of

1:46:44doesn't go with it like maybe um the

1:46:47patient

1:46:48no cremasteric reflex but they have a

1:46:51fever and when you raise the scrotum

1:46:56it's the pain is relieved so there's

1:46:59contradictory information then what they

1:47:01want you to know is what the next

1:47:04diagnostic test is would be a scrotal

1:47:06ultrasound a Doppler to check for blood

1:47:10flow or to narrow the differentials if

1:47:12it's very clear then the next step is um

1:47:17or key opec c so surgery and you want to

1:47:20do bilateral or key epoxy because the

1:47:22other one will most likely towards as

1:47:24well sometime in the future

1:47:27epidural mitos is also i wanna compare

1:47:31and contrast that with or t itis right

1:47:35testicular inflammation of the testicles

1:47:38versus prostatitis so the three of those

1:47:42are all kind of can all get inflamed and

1:47:45in a young person the difference is

1:47:49between a young person and the old

1:47:50person so a young person the main

1:47:52culprits will be gonorrhea and chlamydia

1:47:54and in an older person the main culprit

1:47:58will be e coli so you treat them with

1:48:02different antibiotics by young

1:48:04it's like someone less than 35 and by

1:48:07older like older than 35 and and sexual

1:48:10history helps too so a young person

1:48:13you're gonna give such ceftriaxone and

1:48:15as a throw Meissen and an older person

1:48:18you want to treat with a fluoroquinolone

1:48:22alright fluids electrolytes so the

1:48:25dreaded hyponatremia algorithm so for

1:48:29hyponatremia the first thing you wanna

1:48:31do is check the osmolarity so normal

1:48:35osmolarity is between 275 and 295 if

1:48:39they're mean they won't give it to you

1:48:41if they're nice they'll give it to well

1:48:43if they're mean you have to know how to

1:48:45calculate it

1:48:46so it's 2 times sodium plus 1 18th

1:48:49glucose plus 1/3 bu n that will give you

1:48:53the serum osmolarity and you have to

1:48:56determine whether it's hyperosmolar

1:48:59isotonic or hypo tonic so above 295 in

1:49:04the middle or below 275 if it's high

1:49:08then this is most likely caused by

1:49:11glucose if it's isotonic then this is

1:49:14called pseudo hyponatremia and it's most

1:49:17likely caused by protein or lipids if

1:49:20it's low this is where the majority of

1:49:23them fall under then this the next step

1:49:26is to check volume status if they're

1:49:30hypervolemic if they're euvolemic or

1:49:32they're hypovolemic and that's that you

1:49:35can check by blood pressure and mucosa

1:49:39to see if they're hypovolemic the hub

1:49:41dry mucosa and low blood pressure and so

1:49:44on so if they're hypervolemic the main

1:49:49causes are CHF cirrhosis or a nephrotic

1:49:52syndrome due to a systemic edema and

1:49:55that's fluid overload and then if it's

1:49:58normal volume the two most common or

1:50:00SIADH and primary polydipsia and if

1:50:04they're hypovolemic the most common

1:50:07causes are diarrhea vomiting or

1:50:11diuretics

1:50:12so after you've just determined the

1:50:17volume status right then you wanna check

1:50:21the urine sodium and the cutoff is 20 if

1:50:24it's above 20 or below 20 as a general

1:50:28rule so the urine sodium is an indirect

1:50:33way of checking how good the kid

1:50:35Zaria how good the kidneys are at

1:50:37absorbing sodium so if the urine sodium

1:50:41is low that means you're absorbing

1:50:43sodium well it's kind of like FINA

1:50:45remember FINA if it's greater than 2

1:50:48then that's most likely intrinsic renal

1:50:51but if it's less than 1 then that's most

1:50:53likely pre renal same concept so if the

1:50:56urine sodium is high then this is an

1:50:59intrinsic kidney disease whereas if it's

1:51:02the urine sodium is low then the sodium

1:51:04is able to be reabsorbed so you know the

1:51:07kidneys are good it's got to be

1:51:09elsewhere for example let's start with

1:51:11if you are hypovolemic right hypovolemic

1:51:16hyponatremia and the urine sodium is

1:51:20high then this is most likely diuretics

1:51:24but if the urine sodium is low then this

1:51:27could be diarrhea or vomiting then if

1:51:32they are euvolemic right hypotonic

1:51:36hyponatremia you have to decide is this

1:51:38SIADH or is this primary polydipsia well

1:51:43SIADH right we'll have um since you're

1:51:47pulling in all the water that will

1:51:49concentrate the sodium a lot right so

1:51:51sodium levels will be above 20 but

1:51:55primary polydipsia it's dilute

1:51:57everywhere even in the blood and the

1:52:00urine so the urine sodium concentration

1:52:03will be really low so the exception here

1:52:06is that in euvolemic hyponatremia

1:52:10hypotonic hyponatremia that one you kind

1:52:13of have to use your logic so the last

1:52:15example would be like a hypervolemic

1:52:18hyponatremia if the urine sodium is

1:52:22above 20 then you know this is some sort

1:52:25of chronic kidney disease or acute

1:52:28kidney injury like acute tubular

1:52:29necrosis but if the urine sodium is

1:52:32below 20 then think CHF cirrhosis or

1:52:36nephrotic syndrome but as in general and

1:52:39then the next thing is why you did why

1:52:41it's important to diagnose this

1:52:43it's important to also know how to treat

1:52:48these cases of hyponatremia and not try

1:52:50to make it as simple as possible and for

1:52:54hyponatremia it goes like this

1:52:57hypervolemic or hype or euvolemic

1:53:00without symptoms hypovolemic without

1:53:03symptoms or hypovolemic with symptoms if

1:53:07their hypervolemic or euvolemic without

1:53:11symptoms the first thing you want to do

1:53:13is water restriction if they're

1:53:16hypovolemic and they have no symptoms

1:53:19then the next thing you want to do is

1:53:22normal saline if they're hypovolemic

1:53:25with symptoms or if their sodium levels

1:53:29are below 120 which is severe

1:53:31hyponatremia this is where you give

1:53:33hypertonic saline which is 3% so

1:53:37symptoms of severe hyponatremia would be

1:53:40like lethargy and like coma or like

1:53:44altered Mental Status

1:53:46then for hypernatremia the algorithm

1:53:51goes like this it's either euvolemic or

1:53:55hypervolemic right hypovolemic again

1:53:59without symptoms or hypovolemic with

1:54:02symptoms and so if the way I think about

1:54:05this is if someone has hypernatremia you

1:54:09wanna water it down right but the

1:54:12problem is when you're watering down

1:54:14hypernatremia you have to do it very

1:54:17gradually because remember high to low

1:54:19the brains will blow so if someone has

1:54:24hypervolemia or euvolemic

1:54:26right they're fluid body total body

1:54:30water is already like up to the brim

1:54:33right and there and their blood is very

1:54:35salty so you wanna give basically free

1:54:39water because there's such a small

1:54:41amount of fluid volume left that you

1:54:45want to make as much of an impact as

1:54:47possible to water down that salt so free

1:54:50water but if they are hypovolemic right

1:54:54with no symptoms then

1:54:57basically you want to give d5 half

1:55:01normal saline and that's because just

1:55:03think of it in terms of gradients of the

1:55:06fluid replacement from being a least

1:55:09salty to most salty right so hypovolemic

1:55:13with no symptoms right which is the

1:55:16middle one is you're gonna give

1:55:17half-normal saline and the reason why

1:55:21the your fluid has a little bit more

1:55:24salt is because you need to replace more

1:55:28volume and because there's so much

1:55:30volume you need to replace it needs to

1:55:32be more gradual could you imagine if you

1:55:34filled this much up with only water then

1:55:37that could be really dangerous you could

1:55:40overshoot so that's why you want to be

1:55:42more gentle with half-normal saline

1:55:45versus the most severe form much as if

1:55:48they're hypovolemic with symptoms then

1:55:51that one is where you give a completely

1:55:54normal saline

1:55:55so half is around point four or five

1:55:58percent saline rape but normal saline is

1:56:010.9 so this is the saltiest of the three

1:56:03options and so this one if they have

1:56:07symptoms you want to be able to give

1:56:09normal saline which gives the most room

1:56:13to add as much fluid as possible while

1:56:16being as gentle as possible so to recap

1:56:20if your hypervolemic or euvolemic right

1:56:24you want to just give free water if

1:56:26you're hypovolemic without symptoms then

1:56:30half-normal saline if you were

1:56:33hypovolemic with symptoms the most

1:56:35severe one then that's when you give

1:56:37normal saline so remember that blood

1:56:40transfusions can cause high post calcium

1:56:43yoona because the citrate in the packet

1:56:45will bind up all the calcium and then

1:56:48this is a classic high-yield - is

1:56:50treatment of hypercalcemia the first

1:56:53step is IV fluids treatment of

1:56:56hyperkalemia the first thing you want to

1:56:58do is look at the EKG if there's EKG

1:57:02changes you want to give calcium Luke

1:57:04me that helps stabilize the cardiac

1:57:07membranes and improve helps prevent

1:57:09arrhythmias you can also give insulin

1:57:12which pushes potassium into the soil but

1:57:15make sure to give glucose with it

1:57:17to keep you keep yourself you glycemic

1:57:19and Chaya Axley also helps to which

1:57:23binds potassium in the gut and helps

1:57:25promote excretion of potassium so hyper

1:57:28magnus emia the first sign of

1:57:31hypermagnesemia is loss of deep tendon

1:57:35reflexes and you treat it with IV

1:57:38calcium gluconate which also stabilizes

1:57:41the cardiac membranes

1:57:43next is the parathyroid hormone axis so

1:57:47remember that primary

1:57:48hyperparathyroidism increase PTH which

1:57:52okay so first parathyroid hormone has

1:57:55three actions one is it works on the

1:57:59bones directly which increases calcium

1:58:02and phosphate release from the bone the

1:58:05second thing it does is it will work on

1:58:08the kidney tubules its itself and that

1:58:13will help increase calcium absorption

1:58:15and promote phosphate excretion so

1:58:20increase calcium decrease phosphate the

1:58:22last action of parathyroid hormone is it

1:58:26works on converting helping convert

1:58:29kalsa dial two kalsa trial and then

1:58:33kalsa trial

1:58:34yeah and then calso trial which is

1:58:37vitamin d3 well then go to the gut and

1:58:41that helps increase calcium and

1:58:44phosphate uptake and then you kind of

1:58:47you know all three sites have different

1:58:50of pluses and minuses but at the end of

1:58:53the day when you total it all up the

1:58:56final balance is that high parathyroid

1:58:59hormone causes hypercalcemia and

1:59:03hypophosphatemia so high PTH high

1:59:07calcium low phosphate you treat

1:59:09hyperparathyroidism primary

1:59:11hyperparathyroidism with a

1:59:14parathyroidectomy also the pth access is

1:59:20there's a feedback loop too and the two

1:59:23things that close the loop that causes

1:59:26negative feedback or high calcium levels

1:59:29and high vitamin d3 levels so if vitamin

1:59:32d3 is high boom PTH will shut down if

1:59:35calcium is high boom PTH will shut down

1:59:38as well so this hormone axis is

1:59:41difficult but once you get the hang of

1:59:44it it's pretty fun so next would be on

1:59:47another scenario be hypoparathyroidism

1:59:49so low PTH will mean low calcium and

1:59:54high phosphate another situation is

1:59:57kidney failure so if someone has kidney

2:00:01failure this is getting more tricky you

2:00:03have to remember that they're no longer

2:00:05able to convert kalsa dial to calcitriol

2:00:09because that's a one of the main

2:00:12functions of the kidney so they aren't

2:00:15able to absorb calcium and phosphate

2:00:18from the gut also the kidney tubules

2:00:21don't work so they have low calcium they

2:00:24can't absorb calcium but they can't dump

2:00:26phosphate either

2:00:28so philosoph eight will be locked up in

2:00:31the body and then basically a PT and

2:00:36then actions on the bone will try to

2:00:39increase phosphate and calcium but at

2:00:42the end of the day when you total

2:00:45everything all up the kidney failure

2:00:48will result in elevated PTH but low

2:00:55calcium and high phosphate why because

2:00:59the phosphate is unable to be excreted

2:01:03and the PTH levels aren't high enough to

2:01:07overcome the deficiencies of the the

2:01:11kidney and the gut from absorbing

2:01:14calcium kidney failure will be high PTH

2:01:17low calcium high phosphate and then

2:01:21there's vitamin d2

2:01:23efficiency which can be just an isolated

2:01:25problem which is do can be due to

2:01:28nutritional deficiencies or

2:01:31malabsorption like in celiac disease or

2:01:33people with pancreatic cancer or cystic

2:01:37fibrosis or some might deficiency these

2:01:40people will have low vitamin d3 and then

2:01:45because of that they won't be able to

2:01:47absorb calcium and phosphorus from the

2:01:53gut and then these people will have a

2:01:58total of low calcium low phosphorus and

2:02:03high PTH because when they have low

2:02:05calcium and low phosphorus the PTH will

2:02:08turn on and then it will try to absorb

2:02:13more calcium but it'll also dump out

2:02:16more PTH so PTH will go even lower and

2:02:19then remember that the main source of

2:02:22increasing calcium levels is the gut so

2:02:25basically people who have vitamin D

2:02:30deficiency will blow everything and then

2:02:33the PTH will turn on to try and

2:02:36compensate for that but it will usually

2:02:38still stay very low the last is squamous

2:02:42cell cancer of the lung remember it can

2:02:44mix PTH RP parathyroid hormone releasing

2:02:49related peptide and then this acts

2:02:52exactly the same like parathyroid

2:02:54hormone so it'll increase calcium and

2:02:57decrease phosphate and then remember

2:03:00since the calcium levels will be so high

2:03:03all the time that will feed back on the

2:03:06actual PTH and then the Pete's actual

2:03:08PTH levels will be low so this will

2:03:11cause high calcium low phosphate low PTH

2:03:15and high PTH RP so remember for

2:03:20mechanical ventilation settings pco2 is

2:03:24controlled by tidal volume and

2:03:26respiratory rate whereas pao2 is

2:03:28determined by fio2 and peep so basically

2:03:33a patient whose

2:03:35mechanically ventilated they'll give you

2:03:37the ABG's they'll give you the pH if

2:03:40it's alcoholic or acidotic and they'll

2:03:42give you the pco2 and the pao2

2:03:45and say and then you have to know what

2:03:49kind of adjustments to make like ah ah

2:03:52if the pco2 is too high right so they're

2:03:56hypoventilating then you want to

2:03:58increase ventilation and the parameters

2:04:01you can change our title volume or

2:04:03respiratory rates so if you increase

2:04:05both of those the patient will blow out

2:04:07co2 more and vice-versa whereas if they

2:04:11have hypoxemia low po2 then you can

2:04:15increase peep or fio2 to help increase

2:04:19the oxygen levels and vice-versa

2:04:21that's a classic question they'd like to

2:04:23ask - so in summary acid-base first

2:04:34thing you want to do is check the pH if

2:04:36it's between seven point three five and

2:04:39four or five that's normal

2:04:41below that as acidotic above that as

2:04:44alkalotic that's the first step the

2:04:47second step is to look at co2 and bicarb

2:04:51so co2 is normal between 35 to 45 and

2:04:57bicarb is normal from 22 to 28 and then

2:05:02remember that low bicarb equals acidosis

2:05:06high bicarb equals alkalosis low co2

2:05:10equals alkalosis high co2 equals

2:05:14acidosis so the first thing look at the

2:05:18pH if it's low you know it's an acidosis

2:05:21you have to determine what is the

2:05:23culprit it can either be bicarb or co2

2:05:26one of them will be in the range that

2:05:30will be acidotic or will be acidotic if

2:05:35it's high co2 boom you got it it's the

2:05:38first thing is it's a respiratory

2:05:40acidosis look at the bicarb next right

2:05:45and the

2:05:46Herman and then the bicarb tells is the

2:05:49metabolic side of the pH right there's a

2:05:52respiratory arm which is the co2 and

2:05:54then the metabolic arm which is based on

2:05:57bicarb and then you and then you are

2:06:01determine whether that's acidotic or

2:06:04alkalotic

2:06:05if it's acidotic then that's mixed

2:06:08respiratory acidosis and metabolic

2:06:10acidosis if it's alkalotic then you know

2:06:14that's compensation because it disagrees

2:06:16with the pH that's kind of just a rough

2:06:19overview of how to calculate acid-base

2:06:22but say you have to know the next best

2:06:25step so if you calculate a metabolic

2:06:27acidosis which means a pH below 7.35

2:06:30right and a bicarb that is below 22

2:06:34right the next best step is to calculate

2:06:38the anion gap sodium - chloride - bark

2:06:41bicarb if it's greater than 16 right

2:06:45then that's an anion gap metabolic

2:06:48acidosis then you think of your mud

2:06:51piles in the morning if it's below that

2:06:53it's non anion gap and the two most

2:06:56common causes are RTA or diarrhea and

2:07:00then RTA can be one two or four which

2:07:03I've talked about earlier and then the

2:07:06next is metabolic alkalosis so if it's

2:07:09metabolic alkalosis which means that the

2:07:12pH is above seven point four five and

2:07:16the bicarb is above twenty-eight then

2:07:21the next best step is you want to check

2:07:23the urine chloride if the urine chlorine

2:07:26is high above twenty then this is a

2:07:28renal problem if it's low then this will

2:07:32be GI problem and then remember that if

2:07:37you want to get more detailed if someone

2:07:40has a metabolic acidosis that's non

2:07:43anion gap how can you tell if this is an

2:07:46RTA problem or a diarrhea is you can

2:07:50calculate the urine

2:07:53gap so basically that's sodium plus

2:07:57potassium - chloride if it is negative

2:08:02negative right GU T then this is a GI

2:08:06loss if it's positive then that is a

2:08:08kidney loss so most likely renal tubular

2:08:11acidosis and that is electrolytes

2:08:16so anemia next best step is calculate

2:08:20reticulate lo site count or MCV helps

2:08:23you narrow down your differential

2:08:25increased reticulocyte count would be

2:08:27like two percent or more that means that

2:08:30the baby red blood cells are being

2:08:32pushed out like crazy to replenish the

2:08:36blood cells that have been dying so that

2:08:38either indicates hemolysis or like

2:08:41splenic sequestration and then the MCV

2:08:43can help you decide whether it's

2:08:45microcytic normal cynic or macrocytic

2:08:48the microcytic s-- would be like fast

2:08:51right iron deficiency anemia anemia of

2:08:53chronic disease side arrow blastic me

2:08:56Mia or thalassemia the normocytic s-- is

2:08:59there's a lot of differentials for that

2:09:01and then the macro said X could be most

2:09:04commonly folate deficiency or b12

2:09:08deficiency cyanocobalamin deficiency and

2:09:12to tell the difference between the two

2:09:14while b12 usually has neurologic

2:09:16problems called subacute combined

2:09:19degeneration which is a problem of the

2:09:22dorsal colon and the upper motor neurons

2:09:25the corticospinal tract on top of that

2:09:27blood markers b12 will have an increased

2:09:30methylmalonic acid whereas b9 doesn't

2:09:33and then other causes of but then this

2:09:37is Mac megaloblastic anemia right so

2:09:39that means macrocytic anemia plus hyper

2:09:42segmented neutrophils whereas macrocytic

2:09:46anemia is not necessarily megaloblastic

2:09:49will have an MCV of greater than 100 red

2:09:53the red blood cells UV is greater than

2:09:55100 but they don't have hyper segmented

2:09:58neutrophils and the most common ones

2:10:00would be alcoholics or some to more

2:10:04zebra ones would be Fanconi anemia and

2:10:08diamond black phantom anemia so Fanconi

2:10:11anemia is the one where you have a

2:10:14hypoplastic thumb and pancytopenia