Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
142 Cards in this Set
- Front
- Back
|
define: perihilar
|
around the root of the lung in mediastinal (center) part of the chest.
|
|
|
what is indicative of CHF on CXR?
|
- cardiac enlargement
- perihilar infiltrates |
|
|
how do you determine a prerenal cause for azotemia, by looking at lab values?
|
- BUN is elevated
- creatinine is normal |
|
|
what is creatinine used to measure?
|
creatinine blood levels may be used to calculate creatinine clearance (ClCr), which reflects the glomerular filtration rate (GFR). The GFR is clinically important because it is a measurement of renal function.
|
|
|
what are normal BUN levels?
|
The liver produces urea in the urea cycle as a waste product of the digestion of protein. Normal human adult blood should contain between 7 and 25 mg of urea nitrogen per 100 ml of blood.
|
|
|
what do you think of when you see an elevated BUN?
|
A greatly elevated BUN (>60 mg/dl) generally indicates a moderate-to-severe degree of renal failure. Impaired renal excretion of urea may be due to temporary conditions such as dehydration or shock, or may be due to either acute or chronic disease of the kidneys themselves.
|
|
|
what do you think of when you see elevated BUN, but normal creatinine?
|
Elevated BUN in the setting of a relatively normal creatinine may reflect a physiological response to a relative decrease of blood flow to the kidney (as seen in heart failure or dehydration) without indicating any true injury to the kidney.
|
|
|
what do you see in lab values for post-renal causes of azotemia?
|
- postrenal azotemia is usually caused by urinary tract obstruction
- rise in both urea and creatinine, with rise in urea being larger than that of creatinine |
|
|
when do you see increased synthesis of urea?
|
- severe burns
- prolonged high fever |
|
|
what do you see with BUN and creatinine levels with renal glomerular disease?
|
- rise in both urea and creatinine, together
|
|
|
what percent of CO goes to the kidneys?
|
25%
|
|
|
name some causes of secondary glomerular disease
|
- SLE
- hypertension - polyarteritis nodosa - DM - Fabry disease |
|
|
what are some histologic alterations you see with glomerulonephritis?
|
1. hypercellularity
2. Basement membrane thickening 3. Hyalinization and sclerosis |
|
|
describe the hypercellularity you see in glomerulonephritis
|
- cellular proliferaion of mesangial or endothelial cells
- leukocytic infiltratoin - formation of crescents |
|
|
what are cresents?
|
- accumulation of cells complosed of proliferating paritetal epithelial cells and infiltrating leukocytes
- epithelial cell proliferation occurs after inflammation, and is thought to be initiated by FIBRIN |
|
|
what is the definition of hyalinization, as seen in the glomerulus?
|
- accumulation of material that is homogeneous and eosinophilic by light microscopy
- by EM, the hyaline is extracellualr and consists of plasma proteins that have come ut from circlating plasma into the glomerulus |
|
|
define diffuse
|
involving all glomeruli
|
|
|
define: global
|
- involving entire glomerulus
|
|
|
define: focal
|
- involving only a proportion of the glomeruli
|
|
|
define: segmental
|
- affecting only a part of each glomerulus
|
|
|
what will you see regarding BUN and creatinine levels with renal tubulointerstitial disease?
|
- severe tubulointerstitial disease (severe enough to cause renal failure) will show a rise in both BUN and creatinine
- creatinine may rise out of proportion to the BUN, particularly in acute tubular necrosis |
|
|
in calcific aortic stenosis, what maes up the nodules of calcium salts?
|
- calcium PHOSPHATE salts
- acellular - stains dark blue with hematoxylin and eosin |
|
|
what makes up kidney stones?
|
- calcium oxalates
- sometimes, magnesium phosphates - sometimes uric acid |
|
|
what makes up hemosiderin depositions?
|
complexed iron
|
|
|
where do most kideny stones form?
|
- in the kidney
- can also arise from the urinary tract |
|
|
what is the etiology of urolithiasis?
|
- affects men more than women
- peak onset: 20-30 years |
|
|
what makes up 70% of all renal stones?
|
- calcium oxalate, sometimes mixed with phosphate stones
|
|
|
what makes up 15-20% of all renal stones?
|
- magnesium ammonium phosphate (struvite)
|
|
|
what makes up 5-10% of all renal stones?
|
- uric acid
|
|
|
what are calcium oxalate stones associated with?
|
- in 5% of patients, associated with hypercalcemia and hypercalciuria
- caused by hyperparathyroidism, diffuse bone disease, sarcoidosis, and other hypercalcemic states |
|
|
how are magnesium ammonium phophate stones formed?
|
- usually formed after infections by urea splitting bacteria, that convert urea to ammonia
- proteus - staphlococci |
|
|
how do large renal stones present themselves clinically?
|
- likely to remain silent
- can present as hematuria |
|
|
how does CN IX regulate blood pressure and rate?
|
- carries info from the carotid sinus to the medulla oblongata
- increased blood pressure causes firing of CN IX |
|
|
what causes cardiac tamponade?
|
- neoplasm
- idiopathic pericarditis - UREMIA - bleeding into pericardial space |
|
|
what are the classic signs of tamponade?
|
- decreased atrial pressure
- increased systemic venous pressure - small, quiet heart |
|
|
what are the clinical signs of cardiac tamponade?
|
- hypotension
- tachypnea - tachycardia - increased JVP |
|
|
what is Kussmaul's sign?
|
- rise in systemic venous pressure upon inspiration
- Ordinarily the JVP falls with inspiration due to reduced pressure in the expanding thoracic cavity. Kussmaul's sign suggests impaired filling of the right ventricle due to either fluid in the pericardial space or a poorly compliant myocardium or pericardium. |
|
|
when do you see Kussmaul's sign?
|
* Cardiac tamponade
* Constrictive pericarditis * Restrictive cardiomyopathy * Pericardial effusion * Right ventricular infarction * Right heart failure |
|
|
do you see Kussmaul's sign in cardiac tamponade?
|
- no
|
|
|
what is pulsus paradoxus?
|
- a fall of more than 10mmHg in the systolic pressure with inspiration
|
|
|
when do you see pulsus paradoxus?
|
- exaggeration of the normal variation in the pulse
- the pulse becomes weaker as one inhales and stronger as one exhales. - cardiac tamponade - lung diseases (e.g. asthma, COPD) |
|
|
describe the mechanism of pulsus paradoxus better
|
During inspiration, both systolic and diastolic blood pressure normally decrease. This is because the intrathoracic pressure becomes more negative, blood pools in the pulmonary vessels and thus left-heart filling is reduced.
When this normal reduction is exaggerated, it is termed Pulsus Paradoxus, meaning that there was a fall in blood pressure and a paradoxical rise in pulse rate |
|
|
describe the pressures within the heart with cardiac tamponade
|
- heart is compressed
- diastolic pressure in each chamber is elevated and equals the pericardial pressure - you get an increase in systemic venous pressure and pulm pressure b/c the heart can't accomodate venous return |
|
|
what are the key physical findings for cardiac tamponade?
|
- jugular venous distention
- systemic hypotension - small quiet heart |
|
|
tell me again, why you get decreased systolic blood pressure with inspiration
|
- during inspiration, you get better filling of the RV b/c of negative intrathoraxic pressure
- this increased RV filling pushes the interventricular septum to the left, thereby impairing LV filling -> smaller CO upon inspiration - this is exaggerated with tamponade, b/c the LV has no room to expand |
|
|
how do you differentiate between Tamponade and Constrictive pericarditis?
|
- look at right atrial pressure recordings
- Tamponade: dampened y descent - Constrictive pericariditis: sharp y descent |
|
|
what is the a wave?
|
- atrial contraction
|
|
|
what is the v wave?
|
- passive filling of the atrial during systole
|
|
|
what is the y descent?
|
- fall of atrial pressures after the opening of the tricuspid valve
|
|
|
what do you see in constrictive pericarditis?
|
- Kussmaul's sign
|
|
|
what agents causes constrictive pericarditis?
|
- used to be TB
- now, mainly idiopathic- months to years following viral acute pericarditis |
|
|
describe the pathology of constrictive pericarditis
|
- after acute pericarditis, any pericardial effusion is gradually reabsorped
- in chronic pericarditis, the fluid undergoes organization -> subsequent fusion of the pericardial layers - fibrous scar formation |
|
|
describe the pathophysiology of constrictive pericarditis
|
- in diastole, blood goes from RA to RV, but quickly reaches filling limit -> systemic venous pressures (Right jugular venous pressures) rise. you get signs of RH failure
- you have impaired LV filling now, and decreased SV, CO, BP |
|
|
why don't you get pulsus paradoxus in constrictive pericarditis?
|
- the negative intrathoracic pressures from inspiration do not transmit throught the rigid pericardial shell to the heart -> do not get inspiratory augmentation of the RV during inspiration
|
|
|
what can be confused with tamponade?
|
- a predominant inferoposterior infarct affecting the RV
- however, you would see Kussmaul's sign in the infarct - you would also see a prominent y descent on catheterization |
|
|
explain the mechanism behind Kussmaul's sign
|
- when you inhale, the negative intrathoracic pressure draws blood into the thorax. this blood cannot be accomodated by the heart in constrictive pericarditis -> distention of jugular veins (the opposite of what usually happens)
|
|
|
what is endocardial fibroelastosis?
|
- a type of restrictive cardiomyopathy
- focal or diffuse fibroelastic thickening around the mural LV endocardium - most common in first 2 years of life - see Aortic valve obstruction in 1/3 of cases |
|
|
what do you see on histology for endocardio fibroelastosis?
|
- regular bands of elastic tissue in thick fibrous endocardium
- cardiac chambers are covered with thick, white endocardium |
|
|
what causes endocardial fibroelastosis?
|
- intrauterine virus infection, possibly with mumps virus
|
|
|
what changes do you see to the myocardium with coxackie virus myocarditis?
|
- seen in dilated cardiomyopathy
- flabby myocardium - patchy areas of hemorrhage - four chamber dilation |
|
|
what do you see with cardiac amyloidosis
|
- usually produces restrictive hemodynamcs
- will see extracellular amyloid deposits on histology |
|
|
what does idiopathic subaortic stenosis produce?
|
- hypertrophic cardiomyopathy
|
|
|
what do you see with Loeffler endocarditis on histology?
|
- eosinophilic infiltrate wtih no increase in elastic tissue
|
|
|
what are normal pressures for the RA?
|
0-8
|
|
|
what are normal pressures for the RV?
|
15-30/0-8
|
|
|
what are normal pressures for the PA?
|
15-30/4-12
|
|
|
what are normal pressures for the lungs/Pulmonary Capillary Wedge pressure?
|
- 1-10
|
|
|
what are the normal pressures for the LA?
|
- 1-10
|
|
|
what are normal pressures for the LV?
|
100-140/3-12
|
|
|
what are normal pressures for the Aorta?
|
100-140/60-90
|
|
|
what is the pulmonary capillary wedge pressure (PCWP) used to measure?
|
- the left atrial pressure
|
|
|
what would you predict with a patient with elevated pulmonary wedge pressure and pulmonary artery pressure?
|
- mitral stenosis
|
|
|
what do you see with temporal arteritis? (what sort of inflammation)?
|
- focal granulomatous inflammation with giant cells
- cranial arteries (branches of the carotid) are usually involved |
|
|
what happens if you don't treat temporal arteritis?
|
- can get involvement of the ophthalmic artery -> irreversible blindness
|
|
|
what type of necrosis is seen in polyarteritis nodosa?
|
- fibrinoid necrosis
|
|
|
where do you see leukocytoclastic vasculitis?
|
- hypersensitivity angiitis
|
|
|
what are other names for leukocytoclastic vasculitis?
|
- microscopic polyangiitis
- microsscopic polyarteritis - hypersensitivity vasculitis |
|
|
which organs are most frequently affected by polyarteritis nodosa?
|
- kidneys
- heart - liver - GI tract - seems to spare lungs |
|
|
what do you see on histology for polyarteritis nodosa?
|
- transmural inflammation of the arterial wall- neutrophils, eosinophils, mononuclear cells
- FIBRINOID NECROSIS - all stages of disease progression may be found in different vessels, or even within the same vessel |
|
|
what do you see with leukocytoclastic vasculitis?
|
- all lesions are of the same age
|
|
|
how do patients present with leukocytoclastic vasculitis?
|
- 'palpable purpura' involving skin, mucous membranes, lungs, brain, heart, GI tract, etc
- skin biopsy is diagnostic |
|
|
where do you see p-ANCA?
|
- microscopic polyangiitis
- leukocytoclastic vasculitis (same thing) |
|
|
how do you differentiate microscopic polyangiitis/leukocytoclastic vasculitis from polyarteritis nodosa?
|
- you will see small vessel involvement with microscopic polyangiitis: necrotizing glomerulonephritis and pulmonary capillaritis
|
|
|
what is Churg-Strauss syndrome?
|
- aka allergic granulomatosis and angiitis
- a variant of polyarteritis nodosa - clincially associated with asthma and eosinophilia |
|
|
what do you see on histology for Churg-Strauss syndrome?
|
- will see necrotizing vasculitis with eosinophilia
- P-ANCA is present in 50% of patients |
|
|
why do you get abdominal pain with Churg-Strauss syndrome?
|
- GI vasculitis
- can also get a skin rash due to dermal vasculitis |
|
|
what are the dominant inflammatory cells in leukocytoclastic angiitis?
|
- neutrophils
|
|
|
what do you see on Monckeberg arteriosclerosis?
|
- calcific deposits in muscular arteries in old people (>60)
- NO NOT ENCROACH ON LUMEN |
|
|
what is the epidemiology of Prinzmetal angina in comparison to unstable angina?
|
- Prinzmetal angina patients are younger
|
|
|
how do you diagnose Prinzmetal angina?
|
- observe spontaneous coronary artery spasm during angiography
- or, you can provoke one using ergonovine or ACh, or telling the patient to hyperventilate |
|
|
how fast is your HR in complete heart block (3rd degree)?
|
- ventricle beats independently at 40 beats/minute
|
|
|
what is the Stoke volume in complete heart block?
|
- stroke volume is increased b/c CO = HR x SV, and the CO stays the same
- you'll have an increased stroke volume (~70mmHg) |
|
|
define: precordium
|
the external surface of the body overlying the heart and stomach
|
|
|
where do you hear friction rubs?
|
- arisez from friction of the parietal and visceral leaflets of a serosal membrane
- associated with inflammatory processes involving the pericardium and pleura |
|
|
when do you hear a mid-systolic click?
|
- mitral valve prolapse
- you have a floppy mitral valve b/c of myxomatous degeneration of the leaflets - floppy valve prolapses during systole -> click |
|
|
when do you hear a systolic murmur radiating to the neck?
|
- aortic valve stenosis
- caused by calcification of aortic cusps |
|
|
which drugs cause drug induced lupus?
|
- procainamide
- hydralazine - chlorpromazine - isoniazid - methyldopa - quinidine |
|
|
what are some side effects of procainamide?
|
- class IA antiarrhythmic
- agranulocytosis - bone marrow depression - neutropenia * hypoplastic anemia - thrombocytopenia |
|
|
what are signs of digoxin toxicity?
|
- nausea
- vomiting - anorexia - yellow-green halos in the visual field - cardiac arrhythmias |
|
|
what are the side effects of disopyramide?
|
- class IA agent
- atrial tachyarrhythmias - heart block - conduction abnormalities |
|
|
what are the side effects of flecainide?
|
- paresthesias
- ataxia - flushing - vertigo - tinnitus - depression - worsening of cardiac arrhythmias |
|
|
what are the side effects of Mexiletine?
|
- class IB agent
- palpitations - chest pain - CHF - edema - arrhythmia - tremor - nervousness - blurred vision - CNS stimulation - convulsions |
|
|
what are the major criteria for diagnosing heart failure?
|
- paroxysmal nocturnal dyspnea
- neck vein distension - rales - cardiomegaly - S3 gallop - increased venous pressure - posiive hepatojugular reflex - acute pulmonary edema |
|
|
what is furosemide used for?
|
- heart failure
- edema associated with CHF - hepatic cirrhosis - renal disease - hypertension |
|
|
what are some changes you can get with long-standing, moderately severe anemia?
|
- fatty change of:
- myocytes - renal proximal convoluted tubule cells - centrilobular hepatic cells - degeneration of neurons in cerebral cortex and basal ganglia |
|
|
when do you typically see fibrinous pericarditis?
|
- after MI
|
|
|
what can very severe anemia cause?
|
- frank MI
- particularly if superimposed on an additional hypoxic insult (e.g. hemorrhage, shock, pneumonia) |
|
|
what are Osler's nodules?
|
- purplish or erythmatous subcutaneous papules or nodules in the pads of the fingers and toes
|
|
|
what do conjunctival hemorrhages in a patient with unexplained fever point to?
|
- infective endocarditis
|
|
|
what are the HACEK organisms?
|
- organisms associated with infective endocarditis
- Haemophilus - Actinobacillus actinomycetemcomitans - Cardiobacteriumhominis - Eilkenella - Kingella Kingae |
|
|
what is the treatment for HACEK endocarditis?
|
- ceftriaxone
|
|
|
what are the side effects of ceftriaxone?
|
- usually given after HACEK endocarditis
- eosinophilia (6%) - thrombocytosis (5%) - leukopenia (2%) |
|
|
when do you see red man syndrome?
|
- patients on vancomycin
|
|
|
when do you see reddish-orange saliva?
|
- patients on rifampin
|
|
|
when do you see serum-like sickness?
|
- children on cefaclor
|
|
|
what is cefaclor?
|
second-generation cephalosporin antibiotic used to treat certain infections caused by bacteria such as pneumonia and ear, lung, skin, throat, and urinary tract infections.
Contents |
|
|
what can be used to maintain the patency of the ductus arteriosus?
|
- prostaglandin E
|
|
|
what are glucocorticoids used for in the neonate?
|
- accelerate pulmonary maturation and stimulate production of surfactant
|
|
|
what is the role of insulin on the lungs in a neonate?
|
- inhibits surfactant production
|
|
|
how long does it take for amiodarone to affect atrial fib?
|
- 2-3 weeks
|
|
|
what is Digoxin Immune Fab?
|
- an antibody directed against digoxin
- used in digoxin toxicity |
|
|
what is a papillary firboelastoma?
|
- results from organized thrombi forming on the endocardial surfaces of the mitral valve or LV
- NOT a neoplasm - usually clincially silent - discovered on autopsy |
|
|
what kind of cells make up a cardiac myxoma?
|
- stellate mesenchymal cells within a myxoid background
- found most often in the LA - can produce a ball-valve effect -> mitral stenosis |
|
|
where do you cut to harvest the great saphenous vein?
|
- anterior to the medial malleolus
|
|
|
describe the course of the great saphenous vein going up from the ankle
|
- starts anterior to the medial malleolus at the ankle, and goes posterior to the medial side of the kneee
- then goes through the saphenous hiatus of the fascia lata to empty into the femoral vein slightly below the inguinal ligament |
|
|
when do you see the 'paradoxical movement' of the apex of the heart (LV): outward movement during systole and inward movement during diastole?
|
- when you have a portion of the ventricular wall infarcted
- in this particular case, it's an infaction in the area of distribution hit by the left anterior descending artery |
|
|
which part of the heart is supplied by the circumflex artery?
|
- superior part of the posterior wall
- it anastamoses there with the right coronary artery |
|
|
when would you get increased work for the same stroke volume?
|
- aortic valve stenosis
|
|
|
what is one of the side effects of spironolactone?
|
- K-sparing diuretic (competes with aldosterone in the distal nephron)
- gynecomastia |
|
|
why is infarction less common in leukocytoclastic angiits than in classic polyarteritis nodosa? what sort of cellular involvement do you see?
|
- involves smaller vessels
- fragmentation of neutrophils: leukocytoclasis |
|
|
how is Churg-Strass disease different from leukocytoclastic vasculitis?
|
- Churg Strass is a subtype of polyarteritis nodosa: affects primarily respiratory and renal systems
|
|
|
what is sinoatrial exit block?
|
- skipped beats with the following beat occuring at the correct time interval based on the rhythm that occured before it
|
|
|
what does the suboccipital triangle allow access to?
|
- the vertebral artery
|
|
|
what muscles characterize the suboccipital triangle?
|
- inferior oblique
- rectus major - superior oblique |
|
|
what can albuterol cause at high doses?
|
- tachyarrhythmias
|
|
|
what can glyburide cause at high doses?
|
- used to treat T2DM (tells pancrase to relase insulin)
- at high doses, can cause hypoglycemia |
|
|
what is levothyroxine?
|
- synthetic thyroid hormone
- used to treat hypothyroidism |
|
|
what is montelukast?
|
- a leukotriene inhibitor to prevent asthma attacks
|
|
|
what is kartagner syndrome associated with?
|
- dextrocardia
|
|
|
what is a taussig-Bing malformation?
|
- aorta arises from RV and the pulmonary artery overrides a VSD
|
|
|
what is truncus arteriosis?
|
- single large vessel overlies a VSD
- arises from developmental failure of separatio of teh embryologic truncus arteriosus inot the aorta and pulmonary artery - one great artery receives blood from both ventricles |
|
|
what is a Taussig-Bing malformation?
|
juxtapulmonary ventricular septal defect with malalignment of the infundibular septum.
- The ends of the spectrum are hearts with, on the one hand, double-outlet right ventricle and, on the other hand, a discordant ventriculoarterial connection. |
