uworld details- cardio, pulm, renal Flashcards

Question 1

Q

in what way is the CFTR protein abnormal in cystic fibrosis what is the most common mutation seen

Answer

A

ΔF508 mutation –> impaired post-translational processing of the protein

Question 2

Q

which nephritic syndromes are hypersensitivity reactions? say what type, and what the immunologic actor is

Answer

A

acute post-strep glomerulonephritis = Type III = IgG Immune Complexes Goodpastures Syndrome (a type of RPGN) is a Type II = IgG and IgM complement activation

Question 3

Q

what are the retroperitonial structures what does it mean to be intra vs retroperitonial in terms of 1. movement and 2. surgical access

Answer

A

SADPUCKER: supra-renal glands, aorta (/IVC), duodenum (2nd and 3rd parts), pancreatic, ureter, colon (asc and desc), kidneys, esophagus, rectum :intraperitoneum= can move around, retro=stuck to the walls :surgery for retroperitoneum means you only have to get through the abd wall and aponeurosis to get there, no need to cute through a peritoneal layer to access

Question 4

Q

what FEV1/FVC ratio is indicative of obstructive lung ds **what is an exception to this rule

Answer

A

FEV1/FVC < 70% expected *asthma: between episodes of asthma attacks, the ratio may be normal (~85%)

Question 5

Q

why is the systemic arterial blood slightly less oxygenated that the alveolar capillary blood

Answer

A

pO2 is slightly lower in the LA and LV as compared to pulmonary capillaries because of the MIXING DEOXYGENATED BLOOD into the oxygenated blood leaving the lungs in the pulm V. this supply of de-oxygenated blood comes from… 1- the blood supply to the lungs (bronchial As) : after supplying the O2, the deox blood is carried from bronchial Vs into the pulmonary V 2- thebesian Vs (smallest Vs carrying the blood returning from supplying the myocardium) also drain into pulmonary V

Question 6

Q

contents of which part of the tubule has the lowest osmolarity

Answer

A

normal times: the CD bc w low levels of ADH, the CD is impermeable to water and so can get v v v hypoosmolar during HYPOVOLEMIC state: DT has lowest osmolality, bc the CD aquaporins are now permeable to water and become v concentrated **PT is always iso-osmolar (300), regardless of state the proximal tubule is always

Question 7

Q

which cells in the kidney produce EPO

Answer

A

peritubular interstitial cells

Question 8

Q

how does CKD affect serum levels of..

Ca

phosphate

PTH

Question 9

Q

what are the normal % findings for FEV1, FVC, and diffusion capacity

Answer

A

FEV1= >80% of predicted

FVC= >75% of predicted

diffusion capacity= >80% of predicted

Question 10

Q

what type of collagen is scar tissue made of? what other anatomic structures are made of this type of collagen?

what are the other types of collagen and what do they compose?

what disease processes are highly associated w the dif types of collagen

Question 11

Q

what is the common presentation of acute pericarditis

what is the most common type, with what PE finding

common etiology?

Answer

A

acute pericarditis presents with midline chest pain, sharp, DECREASES WITH LEANING FORWARD

fibrinous pericarditis is the most common type, associated with pericardial friction rub (most specific finding)

can follow a viral URI

Question 12

Q

common population for hypertrophic cardiomyopathy?

anatomic findings associated with hypertrophic cardiomyopathy are what?

how can this be differentated from physiologic cardiac adaptatio in young athletes?

Answer

A

YA adults, ppl w family hx (AD)

hypertrophic cardiomyopathy:

LA enlargement
LV wall thickens ASSYMETRICALLY, with increase thickening of the septal wall and minimal thickening of the other walls
LV ejection fraction is high (normal = 55-70%)
poorly developed capiilaries in areas of thickened walls, –> areas of chronic ischemia (fibrosis, scarring, inc collagen content)

vs cardiac adaptation: where the LV is enlarged slightly and the slight thickening of the LV walls are symmetric and concentric

Question 13

Q

how does the EKG strip line up to the action potential in the myocytes

how does QRS change with inc HR (i.e. excercise?)

Answer

A

QRS= Na influx, VENTRICULAR depol

T wave= K efflux, VENTRICULAR repol

plateua btwn QRS and T wave= CA influx

QT interval= how long it takes the ventricular myocyte to get through one action potential

P-wave= atrial depol

*QRS duration is slightly decreased with inc cardiac conduction velocity (i.e. excercise)

Question 14

Q

how does the lung age over time, and how does this relfect on PFT findings

Answer

A

> 35 yo …

decreasing chest wall compliance from back stiffness/rib calcification
inc lung compliance from loss of elastic recoil, esp in alveolar ducts (uniformly across, unlike emphysema)

–> inc residular volume without any inc in total lung capacity

–> (forced) vital capacity decreases as RV takes up higher proportion of TLC

Question 15

Q

what drugs are in each class of antiarrhythmics?

how do each of the classes of antiarrhythmics effect the EKG?

which ones are use dependent? what does that look like on EKG?

Answer

A

CLASS 1= use dependent (have their effective change on the EKG increase with increased conduction velocity (use) of the heart)

inc QRS duration without changing the QT interval or conduction velocity (bind Na channel)

CLASS 2: beta blockers= dec SA and AV node acitivty so only change EKG in pacemaker cells

prolong PR interval

CLASS 3: delay K out for repol

= prolong QT interval, prolong action potential itself without effecting the conduction velocity

CLASS 4: CCBs= slow down conduction velocity via prolonging AV node repol = prolonged PR interval

Class1: procainamide, disopyrimide quinidie : lidocaine+mexillitine: propafenone+flecainide

Class2: beta blockers

Class 3: amiodarone, dofetilide, ibutilide, sotalol

Class 4= CCBs

CLass 5= other= digoxin, adenosine, magnesium

Question 16

Q

who are the class 1 antiarrhythmics and what are their effects ion channels, depolarization, and action potential (in gen and relative to each other)

Question 17

Q

MOA of digoxin

when is digoxin indicated

Answer

A

increase myocardial contractility: via directly binding Na/K ATPase –> dec Na efflux –> secondary dec in Ca efflux from the cell –> inc Ca-troponin C binding –> inc actin-mysosin bridge formation

digoxin= used to increase inotropy of heart

improve sx of acute, decompensated HF due to LV systolic dysfunction
inc parasympathetic tone and dec AV conduction velocity (helps w cardiac function in pts w rapid ventricular rate)

Question 18

Q

most likely area of injury to the aorta after a major deceleration (i.e. MVA) that causes torsional force and extreme stretching

clin presentation/prognosis

Answer

A

at the aortic isthmus, where it is held by the ligament of triets (usually the most rigid part of the aorta

>80% pts die from aortic rupture before reaching the hospital: survivors have nonspecific CP/back pain, SOB, and may have a widened mediastinum on CXR

Question 19

Q

describe the clin presentation and EKG of A fib

Answer

A

clin= tachy, palpitations, irregularly irregular

often preceded by acute illness or inc sympathetic tone or Holiday Heart Syndrome (inc alc intake)

EKG= irregularly irregular w varying R-R intervals, abset P wave, , narrow QRS, MAY have fine fibrillatory waves (small, irregular waves between QRS show atrial contractions being weird)

Question 20

Q

describe the EKG of ventricular hypertrophy

what is the most common clinical presentation

Answer

A

high QRS in the precordial leads (chest leads, V1-V6)

most commonly presents in untreated HTN

Question 21

Q

in what conditions will you see a prolonged QT interval ?

Answer

A

Torsades des Pointe (aka polymorphic ventrcular tachycardia)

sudden cardiac death

chronic heavy alcohol use

Question 22

Q

acute ischemic colitis

presentation

etiology

what secondary physiologic effects result from the ischemia

Answer

A

= crampy abd pain folloed by hematochezia, mild diffuse abd pain with decreased bowel sounds and inc colonic thickness on imaging w *no enhancement w contrast*

=associated w elderly

-thumbprint sign on imaging= mucosal edema/hemorrhage (i.e. embolism from A-fib, athersclerotic plaque)

=reduction in intestinal blood flow–> ischemia

often @ watershed areas= splenic flexure and distal colon

ischemic tissue leads to build up of lactic acidosis –> renal ammoniagenesis via glutamine metabolism

-too much ammonia production can lead to chronic acidosis, usually will be chronicall compensated too

Question 23

Q

which amino acid is metabolized in ammoniagenesis

where does this take place

Answer

A

kidney

glumatine –> ammonium and bicarb

Question 24

Q

antidote to norepinephrine induced tissue necorsis (OD/leak –> inc vasoconstriction–> tissue necrosis)

Answer

A

inject phentolamine into the area within 12 hours

=potent vasodilator

Question 25

Q

how does transplant rejection of lung present if its a chronic rejection?

where is the damage being down anatomically, be specific

-histo of hyperacute and acute rejection?

Answer

A

= submucosal inflammation in the walls of SMALL AIRWAYS (small bronchioli –> airway obstruction and obliteration –> bronchiolitis obliterans

present w slowly developing dypsnea and dry cough over months to years

hyperacute: general hemorrhage and ischemia = ‘white graft reaction’
acute: inflammatory infiltrate into small blood vessels that can extend into the alveolar walls

Question 26

Q

at what point in time after cessation of BF to an area of myocardium (ligation, thrombus, etc) does the cell stop contracting?

Answer

A

within seconds, the myocardium swtiches to anaerobic metabolism (no longer use ATP), thus stops contracting

Question 27

Q

outline how LV dysfunction can lead to the formation of heart failure cells

Answer

A

x forward push from LV–> backing up and incr hydrostatic pressure in pulmonary capillares –> extravasation of RBCs + extravascular hemolysis –> the remains are phagocytosed by the Møs in teh alveoli and the hemoglobin iron is converted to hemosiderin ==> hemosiderin laden Møs, with prussian blue staining revealing golden brown cytoplasmic infiltrates that turn dark

these Møs in the alveolar parenchyma are called heart failure cells

(the process can happen anywhere, but the name is for when it happens in the alveoli)

Question 28

Q

how does ToF present,

what proess failed to happen embryologically

what are the components of ToF

Answer

A

cyanotic newborn w mild-mod respiratory distress

continous machine line murmur (bc cannot survive without a PDA) heard between scapulae

elevated lactate

-aorta is ANTERIOR, INFERIOR, AND TO THE RIGHT of the pulm A

=failure of spiralization

=VSD, Pulm Valve stenosis, overriding Aorta (in front and on right of), thick RV wall (hypertrophy)

****ToF= ~ToK~ where yall always wanna be right

R (pulm) valve stenosis, R ventrical wall thick, R sided aorta, R ventricle connect to left via VSD******

Question 29

Q

what is the presentation of digoxin toxicity

when would digoxin be used over the first line therapies (CCB/B-bloackers) in a-fib

Answer

A

digoxin is a common second line trx in pts w systolic dysfunction

p non-specific sx, can cause lots of kinds of arrythmias (AV blocks, bradycardia,), abd pain, N, fatigue,

VISUAL COLOR CHANGES

-HYPER-KALEMIA can present in digoxin toxicity (from the inc Na-K ATPase inhibition)

Question 30

Q

urinary tract obstruction, like from a stone, will lead to increased pressure going back up.. what is the specific change(s) seen in the kidney

Answer

A

increased tubular hydrostatic pressure –> dec GFR (as teh hydrostatic P in the glonerulus no change so the gradient diminishes)

Question 31

Q

how does R brachiocephalic V obstruction present

what can cause this

Answer

A

swelling of the R arm and face

-apical lung tumors, thrombotic occlusion, central catheter placed in too long

Question 32

Q

when do you give mom prophylactic trx for neonatal Grp B strep infection

Answer

A

intrapartum penicillin (ampicillin= secondary if allergic)

= during childbirth

Question 33

Q

describe the timeline of tissue changes that occur in the heart after a myocardial infarction

when does the ischemic injury itself start after the onset of oxygen deprivation (i.e. due to coronary A blockage)

Answer

A

(ischemic injury begins w/in 3-4 mintes of O2 deprivation)

0-4 hours = no changes

4-12 hours= wavy fibers w narrow, elongated myocytes

12-24= myocyte hypereosinophilia w pyknoti nuclei

1-3 days= coagulation necrosis (lose nuclei and striations), w prominent neutrophilic infiltrate

3-7 days= disintegration of dead neutrophils and myofibers + Mø infiltrate at the borders

7-10 days= robust phagocytosis of dead cells by Møs, beginning formation of granulation tissue at margins

10-14 days= well developed granulation tissue w neovascularization

2wks-2months= progressive collagen deposition and scare formation

Question 34

Q

hyperhomocysteinemia is an independent risk factor for what kinds of pathologies?

how does the body usually metabolise homocysteine?

what are the causes of of hyperhomocysteinemia?

Answer

A

=independent risk factor for thrombotic events, i.e. DVT.., probs bc of endothelial injury

-usually turned into cystathione OR

homocystein –methylene tetrahydrofolate –> methionine

(above enzyme regenerated via methylene tetrahydrofolate reductase (MTR)

hyperhomocysteinuria associated with decreased metabolism, secondary to enzyme and vitamin deficiency
needs Vit B12 (cobalamin) cofactor to be broken down : also low levels folate (B9), pyridoxine (B6)
genetic xMTR is the most common

Question 35

Q

outline the physiological response that takes place in the kidney in response to decreased renal A pressure in order to maintain GFR

Question 36

Q

describe the changes in GFR seen over time in diabetic nephorpathy and the reason why these changes are seen

how does this affect albuminurua

Answer

A

at first GFR rises, years 5-10 it plataeus, but by year 15 the GFR actually starts to fall

early: inc glucose filtered load–>inc sodium resorp vai Na/glucose antiporter in PT–> set off RAAS–>affarent dilation and efferent constriction–> inc GFR

5-10 years: chronically elevated intraglomerular capillary P will lead to glomerular structural changes–> loss of albumin

10+: widespread glomerulosclerosis –> dec GFR

Question 37

Q

why does the urine dipstick sometimes show (-) proteinuria when a different test will show (+) for proteinuria

Answer

A

conventional urinalyses does not pick up microalbuminuria

need to secrete >300 mg/day of albumin for it to show up on the urinalyses

Question 38

Q

in patients with low HDL levels, what is the MOA of treatment that will actually decrease the risk of CV disease

which drug class is indicated for lowering risk of CV ds regardless of lipid levels

Answer

A

can’t just inc the HDL levels: need to decrease the LDL levels in order to dec risk of CV ds

VIA STATINS

Question 39

Q

how does each of the following affect LDL, HDL, and serum TG levels

statins

fibrates

bile acid sequestrins

niacin

ezetimibe

omega 3- fatty acids

excercise and weight loss

Question 40

Q

statins

indications

MOA

main effects

AE

Answer

A

atorvastatin, simvastatin, rovustatin

ONLY LIPID LOWERING DRUGS PROVEN TO DEC RISK OF CV DS
give after an MI regardless of chol levels, also used as secondary prevention of ds w inc risk i..e DM, hx stroke/TIA

MOA= work @ liver

inhibit HMG CoA-Reductase in the liver–>

dec endogenous cholesterol production in the liver
inc LDL-R expression on hepatocytes

main effects:

-dec LDL

AE=

myopathy = proximal, symmetrical M wk/sore w/in wks-months of starting trx
teratogenic
inc CK, mild inc LFTs(reversible)

Question 41

Q

bile acid sequestrins

indications

MOA

main effects

AE

Answer

A

= cholesteyramine, colesvelam, colestipol

use in conjunction w statins to dc LDLs

MOA= work in intestines and liver

-interrupt enterohepato circulation by inibiting the reabsorption of bile acids in the intestines –> inc endogenous chol production via UPREGULATION of HMG-CoA Reductase (to have chol to make bile salts with) + inc LDL-R on hepatocytes

main effects: dec LDL in circulation

AE=

slight inc TGs and VLDLs (when you inc chol production) = contra in pts w high TGs
inc risk of cholesterol bile stones
constipation and bloating = caution in pts w diverticulitis, IBD, cholestasis
steatorrhea: dec absorption of Vit ADEK,

and drugs= digoxin, thiazides, warfarin, aspirin, STATINS

**need to take bile acid sequestrins and statins at least 4 hours apart

Question 42

Q

ezetimibe

indications

MOA

main effects

AE

Answer

A

decrease LDL levels

-used in conjuction with statins

MOA= dec intestinal absorption of exogenous (dietary) cholesterol –> dec cholesterol in chylomicrones –> dec liver access

= UPREGULATE HMG CoA Reductase activity and inc LDL-R expression on hepatocytes

Main effects= dec LDL levels

AE= inc LFTs, diarrhea

Question 43

Q

fibrates

indications

MOA

main effects

AE

Answer

A

gemfibrizol, fenofibrates

decrease TGs

MOA= work at peripheral tissues and liver

increase expression of PPARalpha-R on liver and peripheral tissues = (+) upregulat lipoprotein lipase (LPL) on peripheral tissues and (-) inhibit inhibitors of lipolysis ==> inc uptake of TGs and VLDL @ peripheral tissues
dec secretion of VLDL by liver –> dec VLDL (–> slight dec LDL)
directly inc synthesis of ALP I + ALP II by hepatocytes –> modest inc HDL

main effects = dec serum TG levels

-slightly dec LDL, slightly inc HDL

AE=myopathy (inc risk w co-admin of statins), modest inc cholesterol bile stones (caution in Fs, obese pts)

Question 44

Q

niacin

(as a lipid lowering drug)

indications

MOA

main effects

AE

Answer

A

aka vit B3

=most effective agent at lowering HDL, also used to lower TGs

MOA=

–inc HDL via (1) dec HDL chol transfer and (2) delay HDL clearance

–dec TGs via dec (1) circulating VLDL secretion from liver and (2) TG release from adipose

–dec LDL via dec in VLDL

main effects: dec TGs and HDL

AE= use limited by poor tolerability

-benign flushing (cutaneous vasodilation) and inflammation via prostoglandins (give NSAIDS prophylactically)

–inc glucose (caustion in diabetics)

-inc uric acid –> gout precipitation (prophylactic trx w allopurinol)

–inc LFTs= MUST REGULARLY MONITOR NIACIN LEVELS TO AVOID jaundice, severe hepatotoxicity, and fulminant hepatitis

Question 45

Q

which cholesterol vessles are good and which ones are bad?

why are they so?

which apolipoproteins exist on which cholesterol vessels?

Answer

A

chylomicrons= carry free cholesterol from intestine to liver

—-ALP (A, B, C, E)

VLDL+LDL = BAD = ALP B-100 (b for bad)

—VLDL= main contributor to atherosclerosis

—LDL= those that are not picked up by the liver can penetrate the arerial endothelial later –> atherosclerosis

HDL= good (H for happy)

-extract ‘free cholesterol’ from peripheral tissue using lecithin (LCAT)

–transfer cholesterol esters from LDL and VLDL to be transported back to liver via CHOLESTEROL ESTER TRANSPORT PROTEIN

–directly deliver cholesterol esters to the liver VIA SCAVENGER 1 RECEPTOR

Question 46

Q

how do CO2 levels and O2 levels effect the cerebral blood flow? tie this in with hyper and hypoventilation

Answer

A

hyperventliation –> inc O2 (total O2 and PaO2), dec CO2

—inc CO2= inc CBF (until plataeu)

—inc CO2= dec CBD (until plataue)

**the whole point of hyperventilation is that when you panic, your body is trynna get as much O2 as possible**

Question 47

Q

_____= a harsh systolic murmur heard in the setting of hypertrophic cardiomyopathy (which can be inherited with ___inhertance, mutation of ____)

-how does a hypertropic cardiomyopathy present

Answer

A

mitral regurg

AD xcardiac sarcomere proteins

-most pts are asx w incidental ECG findings;

or exertional dyspnea, CP, fatigue, palpitations, dizzy, syncope, sudden cardiac death from ventricular dysrhythmia

Question 48

Q

describe physiologic effect (afterload/preload), effect on LV blood volume, and murmur intensity changes seen in hypertrophic cardiomopathy with..

valsalva

abdrupt standing

nitroglycerin admin

sustained handgrip

squatting

passive leg raise

Question 49

Q

on renal tubular microscopy, what is each of the following made of and what does it indicate?

hyaline casts

waxy casts

fatty casts

granular casts

WBC

RBC

which of the above is this?

Answer

A

*attached picture is granular, uddy brown casts*

Question 50

Q

of all the venous blood in the body, which V carries the most deoxygenated blood of all? why?

Answer

A

coronary sinus= carries most of the venous blood that had supplied the myocardium (pour into R atrium)

-the myocardium is more efficient than any other tissue in the body at extracting O2 from the blood, bc he need it

—LV is only oygenated during diastole (since the coronary vessels are contracted during systole) so it has to be able to get a lot of O2 out quick

—-the demands on the heart are >>>

Question 51

Q

infective endocarditis from IV drug users occurs at which valve

Answer

A

staph!! aureus!! infect!! tricuspid!!! valve!!

THREE PYRAMIDS

DONT BE STUPID

Question 52

Q

coarctation of the aorta affects what part of the aorta, typically

while very severe coarctation of the aorta can present in ___ with ____ , moderate coarctation may present ____ with ____.

coarctation of the aorta can be associated with ____ syndrome

Answer

A

typically the region just distal to the L subclavian A

severe: infancy

–cyanosis of LE if ductal arteriosus is open, shock and death if its closed

moderate: childhood or adolscence

–LE extremity claudication (pain and cramping w excercise), BP discepency between UE and LE, and delayed/diminished femoral pulses

-restricted circulation can lead to PULSATILE INTERCOSTAL As and continoues murmurs

associated w Turner Syndrome (up to 10% of Turner pts)

Question 53

Q

what effect does endothelin-1 have on BVs? how is it effected by the RAAS system

Answer

A

endothelin-1 causes vasoconstriction

it is increased when the RAAS system is activated

Question 54

Q

what is the pathophysiology of supine hypotension syndrome

Answer

A

=norm BP when sitting and standing, but fall in BP when supine

=compression of IVC–> dec venous return

Question 55

Q

hyponatremia with a high urine osmolality indicates what pathology?

what are the causes? be specific!

Answer

A

SIADH

CNS disturbances = stroke, hemorrhage, trauma

medications= carbamezapine (anticonvulsant), SSRIs, NSAIDs,

lung ds= pneumonia

malignancy= small cell lung cancer

Question 56

Q

what medication is the preferred antihypertensive trx given to diabetics to mitigate the risk of progression to diabetic nephropathy

Answer

A

ACE Inhibitors/ARBs

along w glycemic control

Question 57

Q

in the setting of metabolic acidosis, what lab values indicate that the cause is diabetic ketoacidosis

how are these labs fixed

Answer

A

give insulin and fluids to…

inc bicarb
inc serum Na
decrease serum osmolality
dec serum K

Question 58

Q

pt presents w dysuria, nausea, fever, and confusion, (+) flank pain. hx of recurrent UTIs. this is their kidney..

what is the probable diagnosis?

pathophys?

Answer

A

das a staghorn calculi
associated w recurrent upper urinary infection from Klebsiella or Proteus = urease producing organisms
the kidney also shows xanthomatous changes in the renal pelvises and atrophy of the cortex

hydrolysis of ammonia via urease –> increases urine pH–> precipitation of magnesium ammonium phosphate salts

Question 59

Q

how do acid base changes affect K levels

Answer

A

alkalosis = hypoK “Ka-LOSE-is” = shift K intracellular

acidosis = hyperK –> shift K extracellular

-

Question 60

Q

this CT shows what?

in and old person w a hx of smoking and exertional dyspnea, what dx is suspected?

Answer

A

dilated airspaces

centriacinar emphysema

Question 61

Q

what organisms can trigger a COPD exacerbation

Answer

A

virus = rhinovirus (common cold), influenza, parainfluenza (generic URI)

bacterial= H. influenza, Moraxella cattarhalis, Strep pneumoniae

Question 62

Q

what is seen in this picture?

what is the correlating pathology?

Answer

A

pleural blebs

centrilobular bullous emphysema

-loss of alveolar elasticity results in alveolar distension.

–in severe cases, large airspaces > 1 cm in diameter form, mostly in the apex = subpleural blebs. if these rupture, you can get a pneumothorax = severe respiratory distress that quickly leads to a sudden death

Question 63

Q

embryologic origin of the kidney

Answer

A

metanephros (split into two parts at some point)

metaneprhic blastema= distal convuluted tubule

metanephric diverticulum aka ureteric bud= the rest of the collecting tubules and ducts, major and minor calyces, rena pelvis, ureters

Question 64

Q

what does the mesonephros give rise to?

Answer

A

in males it becomes the –> wolffian ducts ==> ductus deferens and epididymis

in females, regress and become Gartner’s ducts

Answer 59

A

ADH makes the CD permeable to urea so that it can be resorbed and used in teh medulla to make it more concentrated for the purposes of the loop of henle.

ADH directly decreases the renal clearance of urea

Answer 60

A

–antecedant diarrheal illness (often bloody)

=Shiga-like toxin (Shigella and E. ColiO157:H7)

–hemolytic anemia with schistocytes

=low Hgb, low haptoglobin, pallor, etc.

–thrombocytopenia

=low platelets

–acute kidney injury

=oliguria/anuria, inc Cr, BUN/Cr<20, proteinuria, hematuria

HUS= Hemolytic (anemia, thromboxytopenia), Uremic (AKI), Shiga

Answer 61

A

primary hyperaldosterone= high ALD, low renin

= adrenal tumor/hyperplasia

secondary hyperaldosterone= high ALD, high renin

= renal A stenosis, diuretics, malignant hypertension (via renal ischemia), juxtaglomerular cell tumor (reninoma),

Answer 62

A

mannitol= an osmotic diuretic = it inc the osmolallity of the PT/LoH in order to increase diuresis (water flow into the tubules).

its often used to treat trauma patients with cerebral edema and increased intracranial P

overaggressive trx can –> too much depletion and hypernatremia
also: pulmonary edema via too quick of an increase in hydrostatic P in the vasculature –> plus continued work to inc plasma osomlalit will then pull water out of brain –> death

Answer 63

A

thiazides

Answer 64

A

sirolimus, tacrolimus, cyclosporine

can be used for immunosuppresion post organ translplant

Answer 65

A

eosinophilic invation of the lungs in response to parasitic infection

Answer 66

A

Ascaris infection

(helminth- roundworm)

Answer 67

A

eosinophils

contains granules full of “major basic protein” which is effective against helminths (parasitic worms)

–>release of MBP can also cause endothelial damage in the lung –> chronic lung damage

Answer 68

A

pneumonia, bacteremia, meningitis, epiglottitis

Answer 69

A

lower respiratory infection

almost always viral in etiology = RSV, rhinovirus, influenza, parainfluenza

***NOT H. influenzae**

Answer 70

A

destruction of alveoli–> obstructed air from leaving..

inc TLC (trap)

dec FEV1/FVC (trap)

dec DLCO (loss of alveoli)

Answer 71

A

most: umbilical V–> IVC
least: umbilical A

Answer 72

A

hamartoma aka pulmonary chondroma

=islands of mature hyaline cartilage, along w some fat and sm M, lined by respiratory epithelium

=incidental finding on x-ray, w “popcorn calcification” (well defined coin lesion)

Answer 73

A

mucociliar clearance (cilia of epithelial cells)

end in terminal bronchiols :

respiratory bronchioles have macrophages, alveoli have TII pneumocytes

Answer 74

A

calcitriol = absorb Ca from stomach

calcitonin= put Ca in your bones (inhibit osteoclasts)

Answer 75

A

CKD= dec GFR = dec phophate filtration = inc phosphate levels in serum

inc phosphate = put Ca in your bones= reduce serum free Ca

+phosphate will activate osteocytes+clasts to release FGF-23

inc (phosphate + FGF-23) –> inc calcitriol to also ‘help’ dec serum Ca by xCa resorp in intestine

==> hypoCa ==> secondary hyperPTH–> inc bone turn over –> over time =osteitis fibrosa

Answer 76

A

acute pulmonary edema= i.e. post MI

-see just transudate that makes up the pulmonary edema = acellular, pink paterial

chronic lung congestion=

hemosiderin laden Møs, = heart failure cells
only happens once the capillaru damage is so bad that RBCs leak through and then the Møs are able to digest the exudate (RBCs)

Answer 77

A

infective endocarditis

-can be in young people!

immune complexes from the infection can form and cause DPGN, and cause acute renal insuffieciency (AKI)

Answer 78

A

behind gonadal vessels
infront of external iliac

(enter the true pelvis)

infront of the internal iliac
under the uterine A (water under the bridge)

Answer 79

A

–meningitis

–acute epiglottitis

–septic arthritis (esp in kids!! most common cause in infants!!)

–sepsis

Answer 80

A

=congenital

-a ureter that enters the bladder at the wrong anatomic angle will experience black flow of urine when the bladder is full and/or inc bladder pressure

–> recurrent pyelonephritis

Answer 81

A

acute tubular necrosis= most common type of AKI
=2° to renal ischemia from shock = direct injury to tubular cells

causes=

1) renal ischemia from blood loss/trauma = hypovolemia, upper GI bled,…
2) nephrotoxins=
- abx (aminoglycosides, amphotericin),
- radio-contrast, chemo
- immunosuppressants (cyclosporine, Tacrolimus)
- myoglobin (i.e rhabdomyolysis)

course:

first 36 hrs= initiatory phase= urine output dec, BUN inc
2-6 days= maintenance= urine dec, sign risk of death without trx
2-3 weeks= recovery phase

Answer 82

A

ATN
-K= n
BUN= ↑ (>20)
Cr=n BUN/Cr ration <20
urinalyses= mild hematuria, proteinuria, granular casts + renal tubular epithelial cells in the sediment
= FeNa= >1% (n=1%)

=intrinsic renal ds

cause of azotemia:

direct damage to the tubular epithelium post-ischemia = esp in PT bc of its high ATP requirement
-> sloughed tubular cells and necrotic debris into lumen blocks urinary luminal tract –> back leak –> dec GFR –> azotemia

biopsy: proximal tubular cell ballooning and vacuolar degeneration with morphologically normal glomeruli

Answer 83

A

PATHOGNOMONIC urinalyses findings for Acute Tubular Necrosis (intrarenal) = muddy brown epithelial + granular casts

BUN/Cr <20 = intrinsic *>20= pre-renal

BUN is resorbed in the PT when resorption of Na/water increases in the PT in response to hypovolemia, BUN increases too
but Cr is freely filtered and gets secreted into the tubules, NOT dep on PT, so is not affected

FeNa> 1% = intrinsic renal ( ≤1% = prerenal states)

Answer 84

A

fluid challenge= IV fluids given to pt to restore intravascular fluids
-can be used to differentiate between intrinsic renal and pre-renal ds

=leads to restored renal function in pts w simple prerenal ds
-prs w ATN (intrinsic) = renal dysfunction persists despite fluid challenge

contra in pts w volume overload i.e. heart failure

Answer 85

A

AKI= sudden decline in renal function, defined by ↑ Cr and BUN OR oliguria/anuria

PRE-RENAL azotemia:
=↓ renal BF (i.e. hypotension)–> ↓GFR
–> cause inc Na/H20 + urea retention –> inc BUN/Cr ration (>20) and dec FeNa (<1%), U(Na)<20

INTRINSIC RENAL FAILURE:
= most common from ATN (ischemia or toxins) (muddy, granular casts)
=less commonly from acute glomerulonephritis (RPGN, hemolytuc uremic syndrome)
=or acute interstitial nephritis (drug induced>> infection, AI) (WBC casts, pyuria)
—>U(Na)>40, Fe(Na)>2%

POST-RENAL azotemia=
=due to outflow obstruction = stone, BH, neoplasia, congenital anomalies
=develop ONLY w BILAT obsruction / solitary kidney

Answer 86

A

= AD x PKD1 on chr 16 >>> xPKD2 on ch 14

presentation=
most freq in 20s-50yo
=HTN @ presentation
=chronic flank pain 2° to calculi, UTI, v big kidney
=gross hematuria, nocturia if x concentration ability
=may have microscopic hematuria+proteinuria

extra-renal manifestations:

most common: colonic diverticular ds
hepatic cysts= 50-70% (asx, no effect on liver tests)
∝ berry aneurysms of circle of willis
-> SAH= inc mortality and morbidity
25% have mitral valve prolapse

-most common CD= cardiac causes (cardiac hypertrophy, coronary ds)
-50% develop ESRD by 60 yo, almost all will need dialyses
-variable progression tho,
:worse prognosis with = early dx, M, recurrent infections, proteinuria, HTN, xPKD1

Answer 87

A

Alport Syndrome=
-hereditary nephritis + sensorinueral deafness + glomerular ds + ocular abn

=x α5 subunit of T4 collagen (exists mainly in basal lamina) –> lost size selection in BM, also lost integrity of BM in eyes and ears,
-50% x-linked inheritance, rest are AR or AD

screening=
urinalyses, ophthalmologist, audiologist, skin biopsis

-progress to ESRD by 10-20 yo

Answer 88

A

most common AIN= DRUG INDUCED AIN (rest are infection or autoimmune)

-common causes=
Methicillin (classic)
abx (penicillin, cephalosporin, rifampin, sulfanomides)
NSAIDS (vasoconstriction of afferent glomerular arterioles via x prosoglandins)
PPIs

-sx= nonspecific (wknss, fatigue, anorexia)
may have classic triad of drug hypersensitivity (rash, fever, eosinophilia) - but only 10% have all 3

-urinalyses=
pyuria (pus in urine)+hematuria : inc Cr acutely
WBC casts in the absence of urinary infection
urine eosinophils, mild proteinuria

kidney biopsy findings=
interstitial edema w diffuse cell infiltrate of the interstitum by inflammatory cells
may have tubulitis: may have granulomas 2° to autoimmune causes (i.e. sarcoidosis)

trx: stop the offending agent
- prednisone given empirically

Answer 89

A

fanconi syndrome
= inherited AR renal tubular acidosis of the PT (type 2)
OR= acq RTATII from multiple myeloma, MGUS, waldenstrom macroglobulinemia, or amyloidosis, sjogrens, metal poisonings, drug rxns…

-present w chronic lower back pain, neuromuscular weakness, polydipsia, and polyuria

=multiple PT transport defects–> lots of things leaking into the urine
-in certain settings, see Bence Jones proteins –> crystalline inclusions –> x kidney function
(in setting of MM and waldenstrom globulinemia)

dec bicarb (acidosis), phosphate, and uric acid due to PT dysfunction
HYPO-K (<3.5) :
less PT Na–> inc Na sent to DT –> CD compensate by inc Na/K exchange to resorb Na and send out K
met acidosis –> acidemia–> H/K exchange in cells to bring H into cells and K out into circulation –> inc K filtered load

Answer 90

A

S4

often heard in older adults due to age related dec in ventricular compliance

if loud (like same as the normal heart sounds), probs a pathologically stiff LV –> LV hypertrophy

Answer 91

A

patiromer : cation resin that binds colonic K in exchange for Ca –> trap K in the resin –> excreted in feces

(hyperCa, hypoMg, takes a while to start working (hrs), can bind certain drugs [ciprofloxacin, levothyroxine])

Na zirconium cyclosilicate = a more selective resin, but exchange for Na instead

inc Na = contra w CHF, cirrhosis, etc

Answer 92

A

B1= on cardiac cells and renal juxtaglomerular cells

Gs = inc cAMP

B2= on vascular and bronchial sm M

Gs = in cAMP

Answer 93

A

a vaccine that encompasses many strep pneumo strains

=2 types :

pneumococcal polysaccharide vaccine = contain capsular material from dif strains
pneumococcal conjugate vaccines = contains CONJUGATED capsular materials from dif strains (are attached to protein)

give to children and the elderly who are at risk

Answer 94

A

SA node, right near the opening of the SVC

Answer 95

A

anatomic:

R dominant = R coronary A supplies the posterior descending A
L dominant = L circumflex A supplies the posterior descending A

*PDA = “posterior interventricular A” *

physiologic : the AV nodal A most often arises from the dominant coronary A

associated w MI
AV block

Answer 96

A

external iliac A will become common femoral A once it passes the inguinal L

Answer 97

A

alkaptonuria

=benign childhood ds w severe arthritis in adulthood

=AR xhomogentisic acid deoxygenase

homogentisate –x–> maleylacetoacetate

(part of phenylalanine, tyrosine breakdown)

–> homogentisate will build up –> pigment deposits in CT across the body (sclera, cartliage are easy to see) and in the joints causing v bad arthritis, ankylosing, and motion restriction

—> URINE WILL TURN BLACK WHEN EXPOSED TO AIR

Answer 98

A

LV gallops best heard w a bell over the cardiac apex, pt in left lateral decubitus

-end of expiration is the best time bc the dec lung volume brings the heart closer to the chest wall

Answer 99

A

ToF has a low SVR:PVR ratio –> allow deox pulm blood to flow into systemic vessels –> acute hypoxia

kids will squat to relieve this bc it inc the SVR w/o changing the PVR, so less deox blood flows into the systemic and will go into the pulm A to lungs for oxygenation

*SVR= systemic vasc resist *PVR=pulmonic

Answer 100

A

PFO >> ASD

ASD= aplasia of atrial septum secundum

PFO= incomplete fusion of atrial septum primum and secondum

clinical: either can causes a paradoxical brain embolism

where a VENOUS thrombosis causes embolus to the brain rather than to the lungs

Answer 101

A

cystinuria = AR

young patient w recurrent nephrolithiasis
aminoaciduria aka high level sof cystine in the urine
urine will show flat, yellow, hexogons (the cystine) : the cystine will make cystine stones

Answer 102

A

↓ LV filling
↓ cardiac output
↑ risk a-fib, thromvus formation, tricuspid regurge, JVD, pulm edema
pulm HTN, ↑PCWP –> pulm edema + alveolar hemorrhage

LV hypertroph y∝ aortic valve dysfunction

*MS –> LV dilation**

Answer 103

A

=slit like tear of the LV free wall

rare complication of a transmural MI that

happens either w/in 5 days or up to 2 weeks after the event

*coronary atherosclerosis is often ∝ a transmural MI

Answer 104

A

hydralazine: (preg lady getting into boat)

direct arteriolar vasodilater
may dec renal perfusion
encourage Na+fluid retension
reflex sympathetic activation = not often used (inc heart rate)

fenoldopam (solo witch lady)

D1 -R agonist
arteriolar dilation
renal vasodilation –> inc renal perfusion, inc urine output + natriuresis

Answer 105

A

phenylalanine = selective alpha 1 adrenergic receptor agonist

Answer 106

A

inc cAMP activity –> inc Ca release –> inc HR, inc contractility, inc BP

quick acting

Answer 107

A

nø myeloperoxidase (production of the acid)

Answer 108

A

x titin protein = familial dilated cardiomyopathy

incomplete penetrance : can be

asx to having decompensated heart failure to suddent cardiac death 2° to ventricular arrhythmia

Answer 109

A

syndeham chorea = complication of rheumatic fever

= anti-strep Ab react w basal ganglia

present in acute RF : pts at risk for chronic rheumatic heart ds (valvular ds)

Answer 110

A

inc RBF

inc GFR

dec serum creatinine (bc of inc clearance)

Answer 111

A

asthma

atopy= an allergic reaction that becomes apparent within minutes of exposure in a sensitized individual

Answer 112

A

PP = a drop in SPB > 10 mmHg during inspiration

most commonly caused by cardiac tamponade: can also be caused by severe asthma, COPD, and constrictive pericarditis

PE exam: check for korotkoff sounds (S1 and S2) w steth under BPP cuff

inflate the BP cuff to above SPB and then gradually deflate
note when the K-sounds are first heard only during expiration
note again when they are heard throughout inspo and expo
(note 1 - note 2) > 10 =PP is present

Answer 113

A

pulm As =

sm M thickness= medial hypertrophy
intimal fibrosis
significant luminal narrowing

if sign–> form small plexiforms

trx=

lung resection= definative
trx sx w bosentan (endothelin-R antagonist)= dec pulm A pressure + lessen progression of vascular remodeling and R ventricular hypertrophy

Answer 114

A

ACE inhibitors –> inc bradykinin,

associated w the dry cough

Answer 115

A

left atrium

–LA is the most posterior heart chamber

– use a transesophageal echo to visualize the LA

Answer 116

A

right sided (RINspiration?)

pulmonary and tricuspid

Answer 117

A

asbestosis = dumbbell shaped

= alveolar macrophages will respond – interstitial fibrosis

Answer 118

A

concentric: smaller internal diameter/volume

–aortic stenosis, chronic hypertension

eccentric: larger internal diamter/volume

—aortic or mitral regurge, dilated cardiomyopathy, ischemic heart disease

Answer 119

A

PCWP:

a small balloon is inserted into a small brance of the pulmonary A on its way back to the LA
blow up the balloon to obstruct flow, in time the P will increase to be equal to the pressure inside the LA
NORMAL: LV pressure = LA pressure = PCWP

aortic stenosis:

causes an inc in aortic systolic P, which will increase both LV and LA pressure
both PCWP and LV will inc about the same amount

mitral stenosis

(picture attached: dif from normal only bc the dashed line for L atrial pressure is way vertically displaced upward)
the resistance to BF from LA–>LV will inc LA P without the same inc in LV P so
PCWP will increase, LV will remain n (low)

cardiomyopathy

in both dilated and restricted, the LV and PCWP will both rise, stay relatively similar to each other
dilated = inc both bc x(impaired ventricular contractility)
restrictive = inc both bc x(impaired ventricular relaxation/filling)