uworld details- cardio, pulm, renal Flashcards
details, not gen concepts, that i need to remember
1
Q
in what way is the CFTR protein abnormal in cystic fibrosis what is the most common mutation seen
A
ΔF508 mutation –> impaired post-translational processing of the protein
2
Q
which nephritic syndromes are hypersensitivity reactions? say what type, and what the immunologic actor is
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
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
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
4
Q
what FEV1/FVC ratio is indicative of obstructive lung ds **what is an exception to this rule
A
FEV1/FVC < 70% expected *asthma: between episodes of asthma attacks, the ratio may be normal (~85%)
5
Q
why is the systemic arterial blood slightly less oxygenated that the alveolar capillary blood
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
6
Q
contents of which part of the tubule has the lowest osmolarity
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
7
Q
which cells in the kidney produce EPO
A
peritubular interstitial cells
8
Q
how does CKD affect serum levels of..
Ca
phosphate
PTH
A
9
Q
what are the normal % findings for FEV1, FVC, and diffusion capacity
A
FEV1= >80% of predicted
FVC= >75% of predicted
diffusion capacity= >80% of predicted
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
A
11
Q
what is the common presentation of acute pericarditis
what is the most common type, with what PE finding
common etiology?
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
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?
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
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?)
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)
14
Q
how does the lung age over time, and how does this relfect on PFT findings
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
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?
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
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)
A
17
Q
MOA of digoxin
when is digoxin indicated
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)
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
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
19
Q
describe the clin presentation and EKG of A fib
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)
20
Q
describe the EKG of ventricular hypertrophy
what is the most common clinical presentation
A
high QRS in the precordial leads (chest leads, V1-V6)
most commonly presents in untreated HTN
21
Q
in what conditions will you see a prolonged QT interval ?
A
Torsades des Pointe (aka polymorphic ventrcular tachycardia)
sudden cardiac death
chronic heavy alcohol use
22
Q
acute ischemic colitis
presentation
etiology
what secondary physiologic effects result from the ischemia
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
23
Q
which amino acid is metabolized in ammoniagenesis
where does this take place
A
kidney
glumatine –> ammonium and bicarb
24
Q
antidote to norepinephrine induced tissue necorsis (OD/leak –> inc vasoconstriction–> tissue necrosis)
A
inject phentolamine into the area within 12 hours
=potent vasodilator
25
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?
= 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
26
at what point in time after cessation of BF to an area of myocardium (ligation, thrombus, etc) does the cell stop contracting?
within seconds, the myocardium swtiches to anaerobic metabolism (no longer use ATP), thus stops contracting
27
outline how LV dysfunction can lead to the formation of heart failure cells
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)
28
how does ToF present,
what proess failed to happen embryologically
what are the components of ToF
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\*\*\*\*\*\*
29
what is the presentation of digoxin toxicity
when would digoxin be used over the first line therapies (CCB/B-bloackers) in a-fib
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)
30
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
increased tubular hydrostatic pressure --\> dec GFR (as teh hydrostatic P in the glonerulus no change so the gradient diminishes)
31
how does R brachiocephalic V obstruction present
what can cause this
swelling of the R arm and face
-apical lung tumors, thrombotic occlusion, central catheter placed in too long
32
when do you give mom prophylactic trx for neonatal Grp B strep infection
intrapartum penicillin (ampicillin= secondary if allergic)
= during childbirth
33
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)
(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
34
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?
=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
35
outline the physiological response that takes place in the kidney in response to decreased renal A pressure in order to maintain GFR
36
describe the changes in GFR seen over time in diabetic nephorpathy and the reason why these changes are seen
how does this affect albuminurua
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
37
why does the urine dipstick sometimes show (-) proteinuria when a different test will show (+) for proteinuria
conventional urinalyses does not pick up microalbuminuria
need to secrete \>300 mg/day of albumin for it to show up on the urinalyses
38
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
can't just inc the HDL levels: need to decrease the LDL levels in order to dec risk of CV ds
VIA STATINS
39
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
40
statins
## Footnote
indications
MOA
main effects
AE
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)
41
bile acid sequestrins
## Footnote
indications
MOA
main effects
AE
= 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
42
ezetimibe
## Footnote
indications
MOA
main effects
AE
decrease LDL levels
## Footnote
-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
43
fibrates
## Footnote
indications
MOA
main effects
AE
gemfibrizol, fenofibrates
## Footnote
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)
44
niacin
(as a lipid lowering drug)
indications
MOA
main effects
AE
aka vit B3
## Footnote
=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
45
which cholesterol vessles are good and which ones are bad?
why are they so?
which apolipoproteins exist on which cholesterol vessels?
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
46
how do CO2 levels and O2 levels effect the cerebral blood flow? tie this in with hyper and hypoventilation
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\*\*
47
\_\_\_\_\_= 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
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
48
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
49
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?
\*attached picture is granular, uddy brown casts\*
50
of all the venous blood in the body, which V carries the most deoxygenated blood of all? why?
coronary sinus= carries most of the venous blood that had supplied the myocardium (pour into R atrium)
## Footnote
-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 \>\>\>
51
infective endocarditis from IV drug users occurs at which valve
staph!! aureus!! infect!! tricuspid!!! valve!!
THREE PYRAMIDS
DONT BE STUPID
52
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
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)
53
what effect does endothelin-1 have on BVs? how is it effected by the RAAS system
endothelin-1 causes vasoconstriction
it is increased when the RAAS system is activated
54
what is the pathophysiology of supine hypotension syndrome
=norm BP when sitting and standing, but fall in BP when supine
=compression of IVC--\> dec venous return
55
**hypona**tremia with a **high urine osmol**ality indicates what pathology?
what are the causes? be specific!
SIADH
CNS disturbances = stroke, hemorrhage, trauma
medications= carbamezapine (anticonvulsant), SSRIs, NSAIDs,
lung ds= pneumonia
malignancy= small cell lung cancer
56
what medication is the preferred antihypertensive trx given to diabetics to mitigate the risk of progression to diabetic nephropathy
ACE Inhibitors/ARBs
along w glycemic control
57
in the setting of metabolic acidosis, what lab values indicate that the cause is diabetic ketoacidosis
how are these labs fixed
give insulin and fluids to...
- inc bicarb
- inc serum Na
- decrease serum osmolality
- dec serum K
58
pt presents w dysuria, nausea, fever, and confusion, (+) flank pain. hx of recurrent UTIs. this is their kidney..
what is the probable diagnosis?
pathophys?
- 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
59
how do acid base changes affect K levels
alkalosis = hypoK "Ka-LOSE-is" = shift K intracellular
acidosis = hyperK --\> shift K extracellular
-
60
this CT shows what?
in and old person w a hx of smoking and exertional dyspnea, what dx is suspected?
dilated airspaces
centriacinar emphysema
61
what organisms can trigger a COPD exacerbation
virus = rhinovirus (common cold), influenza, parainfluenza (generic URI)
bacterial= H. influenza, Moraxella cattarhalis, Strep pneumoniae
62
what is seen in this picture?
what is the correlating pathology?
pleural blebs
## Footnote
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
63
embryologic origin of the kidney
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
64
what does the mesonephros give rise to?
in males it becomes the --\> wolffian ducts ==\> ductus deferens and epididymis
in females, regress and become Gartner's ducts
65
how does vasopressin/ADH affect the renal clearance of urea
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
66
what is a normal specific gravity for urine
1.006
67
clinical presentation of Hemolytic Uremic Syndrome (HUS)
--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
68
labs that differentiate between primary and secondary hyperaldosteronism?
causes of each
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),
69
how does mannitol work
indications
AE
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
70
rhabdomyolysis: causes, etiology, lab findings
71
in pts with recurrent nephrolithiasis, what can be given to prevent stone formation by \**decreasing*\* urine Ca excretion
thiazides
72
which immunosuppressive drugs work by blocking IL-2, thereby inhibiting lymphocyte proliferation
what are they often used for
sirolimus, tacrolimus, cyclosporine
can be used for immunosuppresion post organ translplant
73
in what type of cell-cell junctions are cadherins present? connexins?
74
what is Loeffler syndrome
eosinophilic invation of the lungs in response to parasitic infection
75
a pig farmer with cough, dyspnea, and scattered wheezing and crackles, with immune cells present in the lung
what is the likely pathology
Ascaris infection
(helminth- roundworm)
76
which immune cell is meant to fight off parasites
how does it do that
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
77
what \*\*specific\*\* diseases are infants protected from when they are given the Hib vaccine
pneumonia, bacteremia, meningitis, epiglottitis
78
what is bronchiolitis and what is its etiology- be specific
lower respiratory infection
almost always viral in etiology = RSV, rhinovirus, influenza, parainfluenza
\*\*\*NOT H. influenzae\*\*
79
what substances are actively reabsorbed from the PCT? what substances are collected in the tubule to be excreted?
80
how does emphysema change..
total lung capacity
FEV1/FVC ratio
DLCO (diffusion capacity for carbon monoxide)
destruction of alveoli--\> obstructed air from leaving..
inc TLC (trap)
dec FEV1/FVC (trap)
dec DLCO (loss of alveoli)
81
what vessels carry the most highly oxygenated and the least oxygenated (most deox) blood in the fetal circulation
most: umbilical V--\> IVC
least: umbilical A
82
the most common benign tumor of the lung is?
what is its composition?
how does it present
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)
83
what mechanism removes the vast majority of inhaled particles that lodge in the bronchial tree?
how far down do these cell types appear in the tree? what are they replaced w
mucociliar clearance (cilia of epithelial cells)
end in terminal bronchiols :
respiratory bronchioles have macrophages, alveoli have TII pneumocytes
84
what is the function of calcitriol and calcitonin
calcitriol = absorb Ca from stomach
calcitonin= put Ca in your bones (inhibit osteoclasts)
85
what are the levels of the following during CKD
PTH
phosphate
calcitriol
what is the result of these changes over time??
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_**
86
what are the lung findings in acute and chronic pulmonary congestion
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)
87
what is the most cause of fever + fatigue + new onset heart murmur
what renal complication can result from this
infective endocarditis
-can be in young people!
immune complexes from the infection can form and cause DPGN, and cause acute renal insuffieciency (AKI)
88
describe the pathway of the ureteres from the renal pelvis down to the bladder
what vessels does it pass in front of and behind of
1. behind gonadal vessels
2. infront of external iliac
(enter the true pelvis)
3. infront of the internal iliac
4. under the uterine A (water under the bridge)
89
what sicknesses can be H. influezae cause
--meningitis
--acute epiglottitis
--septic arthritis (esp in kids!! most common cause in infants!!)
--sepsis
90
what is the cause of vesicoureteral reflux
=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
91
what is the most common cause of acute kidney injury
what etiologies and substances does it result from (be specific)
what is the course + prognosis of this most common cause
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
92
what lab findings are found in acute tubular necrosis
K
BUN
Cr
urinalysis
Fractional excretion of Na
=pre-renal or intrinsic renal ds??
=what is the cause of the azotemia seen?
what are biopsy findings?
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
93
what lab findings indicate INTRINSIC renal disease rather than pre-renal ds
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)
94
what is the fluid challenge and what does it help determine
when is this challenge contraindicated
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
95
# define acute kidney injury
what are the three categories/types of acute kidney injury
what are the causes of each
differening urine/fractional excretion of Na?
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
96
AD polycystic kidney ds
- mutation
- presentation
- extra-renal manifestation
- prognosis
= 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
97
-hereditary nephritis associated with sensorineural deafness points to what pathology?
- mutation and inheritance
- how is dx made
- course of ds
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
98
what is the most common etiology of acute interstitial nephritis
- most common causes? be specific
- clin presentation?
- typical lab findings?
- typical biopsy findings?
- trx?
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
99
fanconi syndrome
- what is it
- how does it present
- pathogenesis?
- explain the etiology behind lab findings
\*\*what medication given MIMIC fanconi syndrome
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
100
a heart sound heard immediately after S1 (almost attached to the end of S1) is what? occurs when?
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
101
trx for chronic hyperkalemia
AE?
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
102
how do B1 and B2 receptors affect cardiac cells and vascular wall cells?
B1= on cardiac cells and renal juxtaglomerular cells
Gs = inc cAMP
B2= on vascular and bronchial sm M
Gs = in cAMP
103
what pathologies cause inc and dec splitting of heart sound 2
104
what are the effects of the different classes of diuretcs on serum levels of Ca and uric acid
105
what is the pneumococcal vaccine and who is recommended to receive it
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
106
what is the dominant pacemaker of the heart and where is its (specific) location
SA node, right near the opening of the SVC
107
what is the anatomic meaning of a "left or right dominant" circulation of the coronary As?
what is the physiologic significance of the dominance?
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
108
where does the common femoral A come from
external iliac A will become common femoral A once it passes the inguinal L
109
an adult with pain of the spine/multiple joints (worse at end of day), with blue black spots in the sclera and/or auricular cartilage
FH of OA
dx? pathology?
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
110
what is the etiology of hearing gallop S3 and gallop S4?
when are they normal? abn?
how can you hear them best?
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
111
explain the etiology of acute hypoxic spells in Tetrology of Fallot
what maneuver can relieve sx?
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
112
which is more common, ASD or patent forament ovale?
etiology of each?
clinical sign?
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
113
how will patients with cystinuria present
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
114
what are the hemodynamic findings seen in mitral stenosis
what finding suggests noncomitant aortic valve dysfunction
* ↓ 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\*\*
115
what pathologic finding is seen in the autopsy
what is the etiology
=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
116
compare and contrast hydralazine and fenoldopam as trx for hypertensive emergency
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
117
what drug, which works on an adrenergic receptor, causes
* inc peripheral vascular resistance
* inc systolic BP
* dec pulse P
* dec HR
phenylalanine = selective alpha 1 adrenergic receptor agonist
118
what effect does glucagon have on myocytes
inc cAMP activity --\> inc Ca release --\> inc HR, inc contractility, inc BP
quick acting
119
what is the cause of the green/yellow color of sputum ∝ bacterial infections
nø myeloperoxidase (production of the acid)
120
AD x TTN gene is associated with what?
x titin protein = familial dilated cardiomyopathy
incomplete penetrance : can be
asx to having decompensated heart failure to suddent cardiac death 2° to ventricular arrhythmia
121
what is the most common cause of acquired chorea (purposeless jerking) in children
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)
122
how does pregnancy change
renal blood flow
GFR
serum creatinine levels
inc RBF
inc GFR
dec serum creatinine (bc of inc clearance)
123
which obstructive lung ds is associated with atopy
asthma
atopy= an allergic reaction that becomes apparent within minutes of exposure in a sensitized individual
124
what kind of pathologies cause pulsus paradoxis?
what is the PE exam that is done to determine the presence of pulsus paradoxis?
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
125
what is the histology of pulmonary arterial hyptertension
what is the trx of PAH (MOA)
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
126
how do ACE inhibitors affect levels of bradykinin
ACE inhibitors --\> inc bradykinin,
associated w the dry cough
127
enlargment of which heart chamber can displace the esophagus/trachea
left atrium
--LA is the most posterior heart chamber
-- use a transesophageal echo to visualize the LA
128
which murmurs get louder on inspiration
right sided (RINspiration?)
pulmonary and tricuspid
129
what is this pathology? which cell is responsible to the immune response to this?
asbestosis = dumbbell shaped
= alveolar macrophages will respond -- interstitial fibrosis
130
describe the change in the diameter of the space insider the left ventricle with concentric vs eccentric hypertrophy of the LV walls
what conditions lead to either condition
concentric: smaller internal diameter/volume
--aortic stenosis, chronic hypertension
eccentric: larger internal diamter/volume
---aortic or mitral **regurge**, dilated cardiomyopathy, ischemic heart disease
131
what does PCWP directly measure
--how is it affected by aortic stenosis
--how is affected by mitral stenosis
--how is it affected by cardiomyopathy (dilated vs restrictive)
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)
132
abn cardiac pacemaker activity starting at what level will show complete desynchronization of the P wave and QRS wave on ECG
starting at the AV node --\> SA node block with AV node pacemaker activity can show up as 3rd degree AV block (complete)
* SA node firing --\> atrial contraction --\> P wave
* AV node fiding --\> ventricular contraction --\> QRS
* both are not synced at all
133
trx w what drugs should be avoided in patients with hypertrophic cardiomyopathy
those that decrease preload or reduce systemic vascular resistance
* will worsen the dynamic LV obstruction
* = vasodilators (nitroglycerin and nictrates, dihydropiridine CCBs) and diuretics
134
135
136
where in the respiratory tract is mucus produced
in the bronchioles
NOT resp/terminal bronchioles, alveoli. etc...
137
138
from where in the heart do the following originate
* a-fib
* AV node re-entry tachy
* a-flutter
* wolf-parkinson-white (AV re-entrant tachy)
139
what is lipofuscin and when is it seen
