Heme 1 Flashcards
pulseless dz- weak pulses in upper extremities
Takayasu’s arteritis
Takayasu’s arteritis- labs?
ESR is elevated
Takayasu’s arteritis- biopsy?
granulomatous changes in walls of affected large vessels
Anti- IgG seen in? AKA?
AJKA rheumatoid factors. associated with RA
morning stiffness, rheumatoid nodules, etc.
cytoplasmic? -antineutrophil cytoplasmic antibody seen in?
Wegner’s granulomatosis
Wegner’s granulomatosis- characterization
pulmonary and renal focal necrotizing granuloomatois vasculitis
P-ANCA seen in?
polyangitis and churg-strauss
hypertrophic obstructive cardiomyopathy- mode of inheritance?
auto dom in 50% otherwise idiopathic
hypertrophic obstructive cardiomyopathy- micro?
myofiber hypertorphy and disarray
See extensive neutrophilic infiltrate in necrotic myofibers
3-4 days after MI
Lymphocytic infiltration in heart
Viral myocarditis
Aschoff bodies
are collections of lymphocytes, macrophages, and occasionally giant cells in myocardium surrounded by fibrinoid degeneration. pathomneumonic for rheumatic heart disease
Aschoff bodies
are collections of lymphocytes, macrophages, and occasionally giant cells in myocardium surrounded by fibrinoid degeneration. pathomneumonic for rheumatic heart disease
amyloidosis causes what kind of cardiomyopathy?
restrictive.==> leads to ventricular stiffening and imparied cardiac filling during diastole
what is idiopathic hypertrophic subaortic stenosis?
AKA hypertrophic cardiomyopathy
pathophys of microscopic polyangiitis
activation of neutrophils and monocytes by P-ANCA leads to inflammation and etc…
Pregnant woman comes in with norm BO sitting, but super low BP when lying supine…explain.
IVC compression during third trimester of pregnancy because of large uterus. decr. venous return to heart, and hypotension when lying supine. tell them to lay on left side (take uterus off IVC)
How do fibrates work?
Incr HDL levels by increasing PPAR- alpha activity
How do statins work?
inhibit HMG-CoA reductase (which is the rate limiting step in cholesterol synthesis)
Side effects of amiodarone?
hyperthyroidism (which causes weight loss, hyperreflexia, and palpatations) hepatotoxicity, and pulmonary fibrosis
What happens 4 hours after an MI?
coagulative necrosis
When does neutrophilic infiltration happen after an MI?
24 hours after
When does neutrophilic infiltration happen after an MI?
24 hours after
When do mononuclear cells appear after an MI?
7-10 days after
When do fibroblasts deposit collagen after an MI?
2-3 weeks after!
What are the 5 Ts of neonatal cyanosis?
tetralogy of fallot transposition of great vessels truncus arterious tricuspid atresia total anomalous pulmonary venous return
neonatal cyanosis. diabetic mother.
transposition of great vessels
newborn with hypotenstion, tachypnea, single S2, prominent systolic ejection murmur at upper sternal border, and mid-diastolic rumble at left lower sternal border?
pulmonary atresia (presents with early cyanosis as patent ductus arteriosus closes)
newborn with hyperactive right ventricular impulse, quadruple rhythm, fixed and split S2, prominent systolic ejection murmer at left upper sternal border, and mid-diastolic rumble at left lower sternal border
anomalous venous return
what happens in anomalous venous return?
pulmonary veins don’t drain into left atrium, may drain into superior vena cava instead
what is prazosin and what is it used to treat?
alpha 1 blocker, used to treat HTN and BPH
what is prazosin and what is it used to treat?
alpha 1 blocker, used to treat HTN and BPH
what is clonidine and what is it used to treat?
centrally acting alpha agonist use dot treat HTN, especially in renal disease
What is dobutamine? used for?
Beta agonist. used to treat shock and heart fail
what is Mirtazapine and used for?
selective alpha 2 blocker. used for depression. adverse effects include sedation and inreased appetite
what is phenoxybenzamine and used for?
irreversible alpha blocker. used for pheochromocytomas
what is phenylephrine? and used for?
alpha agonist (1 >2) used as nasal decongestant and pupillary dilator
what is intermittent claudication?
painful ischemic condition caused by peripheral atherosclerosis of arteries
what is intermittent claudication?
painful ischemic condition caused by peripheral atherosclerosis of arteries
physio of smooth muscle contraction?
- membrane depolarizes and VG Ca channels open
- calcium binds to calmodulin.
- ca+calmodulin complex activates myosin light chain kinase
- kinase phosphorylates myosin light chains
- the light chains facilitate cross bridge formation and SM contraction
What is Diltiazem and used for?
class 4 antiarrhythmic. prolongs PR interval. esp in AV nodal cells.. useful in preventing nodal arrhythmias
How do Ca++ channel blockers work and what are they used for?
useful for HTN becasue they inhibit Ca++ influx into vascular SM cells. decr. vascular tone
Amiodarone is first line med for what?
V fib after an MI
Would you give a class 1C antiarrhythmic to a post MI?
NOOO! associaed with mortality. it works at phase 3 of action potential and has no effect in AP duration. They’re used in v tachy, or intractable supraventricular tachy
What do you use Procainamide to treat?
it is a type 1A antiarrhythmic. used for V fib. increases AP duration and QT interval. often used for re-enterant and ectopic supraventricular and ventricular tachy.
common side effect of procainamide?
drug induced lupus
digoxin tox?
yellow-green vision, nausea, vomiting, diarrhea, arrythmias.
Digoxin use?
chronic heart failure. control a fib (NOT v fib)
Digoxin mechanism?
inhibits Na/K ATPase. leading to indirect inhibition of na/ca exchanger. incr in intracellular ca. positive inotrophy
familial hyercholesterolemia- inheritance
auto. dom
xanthomas in achilles tendom, arcus lipoides, and very high LDL level…what i it?!
familial hypercholesterolemia or type IIa dyslipidema
xanthomas in achilles tendom, arcus lipoides, and very high LDL level…what i it?!
familial hypercholesterolemia or type IIa dyslipidema
familial dyslipdemia- type 1- hyper chylomicronemia
auto recessive. lipoprotein lipase deficiency altered APO C-II. causes pancreatitis, hepatosplenomegal, eruptive/ ruritic xanthomas no increased risk for atherosclerosis. creamy layer in supernatant
familial dyslipdemia- type 2a- familial hyper cholesterolemia
auto dom. absent/defective LDL receptors accelerated atherlo. (MI before 20) tendon xanthomas corneal arcus
familial dyslipdemia- type 4-hyper triglyceridemia
auto dom
hepatic overproduction of VLDL
may cause acute pancreatitis
Hep B associated with which vasculitis
polyarteritis nodosa.
what type of hypersensitivity is polyarteritis nodosa?
type 3. complex deposition in medium sized vessels ANCA negative
statin + fibrate what side effect?
rhabdomyolysis
pt has high BUN and creatinine, recent oliguria, what do you see on ECG?
acute renal failure, can’t secrete potassium. leads to hyperkalemia. see peaked T waves
bilateral renal artery stenosis….what do you see on ECG?
=> incr in RAS=> incr in aldo => incr in secretion of K=> extreme hypoK => U waves
systolic flow murmur because of high
fixed split S2
ASD, most likely from a patent foramen ovale.
first choice antihypertensive in diabetic
ACE inhibitors! because renal protective
What can a thiazide toxicity cause?
mech: inhibits Na resorption in early DT. Can cause high lipids, uric acid, calcium
What can gitelman syndrome cause?
mimics thiazide tox.
mutation in thiazide sensitive nacl co transporter in DCT.
Hyper GLUC
(glycemia, lipidemia, uric acid, calcium)
Side effect of spironolactone (K sparing diuretic)
gynecomastia. inhibition of androgen receptor signaling
what is libman- sacks endocarditis (LSE)?
associated with SLE. deposition of small sterile vegetations made of fibrin and inflamm cells. may rarely embolize.
what is libman- sacks endocarditis (LSE)?
associated with SLE. deposition of small sterile vegetations made of fibrin and inflamm cells. may rarely embolize.
how does nitroglycerin work?
reduce O2 use by heart and incr O2 supply to heart. (systemic venodilation, dilate coronary vessels
would you give digoxin to pt with acute coronary syndrome?
NO! digoxin is a cardiac glycoside that increases cardiac ionotropy. it will increase O2 demands
what would a carotid sinus massage do?
stim carotid baroreceptors. incr para, and slow HR (decr SA and AV firing rate)
Tx for septic shock
Norepi (priority is to stabalize BP)
Wernike’s aphasia. where is the stroke?
MCA (because Wernike’s is in left superior temporal gyrus)
Wernike’s aphasia. where is the stroke?
MCA (because Wernike’s is in left superior temporal gyrus)
valvular damage, chorea, fever, polyarthritis
rheumatic fever!
How do beta blockers decrease O2 demand of heart?
decr HR, decr contractility, decr afterload, secondary to decreased cardiac output and BP.
Decreased symp tone will decrease inward Na current, slow phase 4 depol, and prolong diastole. the coronary arteries are filled in this phase.
what do alpha receptors do?
vasoconstriction of arteries, increases BP
What do Beta 1 receptors do?
incr contractile force and HR
what unintended side effect does Norepi have and why?
norepi will increase venous return to heart (mostly stimulate alpha 1) by vasoconstriction and increased heart contractility, incr in stroke valume. So there will be reflex bradycardia
