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Summary High Yield World Study Guide - USMLE Step 1
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comprehensive notes on very world learning objective and how often thattopiccomes up on exam day.
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QID Topic Educational Objective System Subject Repeats1 Poststreptococcal PSGN presents most commonly in children w/ hematuria, HTN, and periorbital oedema. RBC casts and mild proteinuria may be present on UA, and serum creatinine may Renal, Urinary & Pathology (Path) 8
glomerulonephritis be ↑. Electrolytes (RE)
2 Congenital anomalies of In horseshoe kidney, the kidneys are fused at the poles. The isthmus of the horseshoe kidney usually lies anterior to the aorta and posterior to the inferior mesenteric artery Renal, Urinary & Anatomy (Anat) 3
kidney and urinary tract (IMA). During fetal development, the IMA limits the ascent of the horseshoe kidney. Electrolytes (RE)
3 Polycystic kidney disease ADPKD is caused by muts in the polycystin genes (PKD1, PKD2), which result in cystic enlargement of the kidneys and progr renal dysfxn. CFx incl HTN, abdo/flank Renal, Urinary & Pathology (Path) 3
pain, and gross hematuria; extrarenal MFxs incl liver cysts and intracranial aneurysms. Electrolytes (RE)
4 Subarachnoid hemorrhage Intracranial BAs of the COW are often seen in pts w/ ADPKD; when ruptured, they cause SAH that presents w/ sudden onset of 'thunderclap h/a'. Nervous (NS) Pathology (Path) 4
6 Tuberous sclerosis Renal angiomyolipoma is a benign tumor composed of blood vessels, smooth muscle, and fat. Bilateral renal angiomyolipomas are associated with tuberous sclerosis, an Miscellaneous Pathology (Path) 1
autosomal dominant condition. (Multisystem) (MS)
7 Anti GBM disease Goodpasture syndrome is caused by auto-Abs against the α 3 chain of type IV collagen in GBM and ABMs (anti-GBM Abs). Pts typically present w/ RPGN (nephritic Renal, Urinary & Pathology (Path) 2
syndrome) and alveolar hemorrhage (SOB, hemoptysis). Electrolytes (RE)
8 Poststreptococcal Poststreptococcal glomerulonephritis is most common in children and presents with nephritic syndrome (eg, renal failure, hypertension, hematuria with red blood cell Renal, Urinary & Histology (Hist) 8
glomerulonephritis casts) 2-4 weeks after an infection with group A β-hemolytic Streptococcus. Immunofluorescence microscopy shows granular deposits of IgG, IgM, and C3 in the Electrolytes (RE)
mesangium and basement membranes.
9 Anti GBM disease Anti-glomerular basement membrane (GBM) antibodies react with collagen type IV, causing rapidly progressive glomerulonephritis with glomerular crescent formation Renal, Urinary & Histology (Hist) 2
on light microscopy. Immunofluorescence demonstrating linear deposits of IgG and C3 along the GBM is characteristic. Electrolytes (RE)
10 Glomerular disorders IgA nephropathy (Berger disease) freq presents as recurrent, self-limited, painless hematuria w/i 5 days of an URI. Kidney biopsy will show mesangial IgA deposits on IF. Renal, Urinary & Pathology (Path) 9
In contrast, PSGN is seen 1-3wks after streptococcal pharyngitis and is usually not recurrent. Electrolytes (RE)
11 Poststreptococcal PSGN is an IC-deposition disease that occurs 2-4wks after exposure to GAS (β-hemolytic) species (e.g. pharyngitis, skin infection). LM shows enlarged, hypercellular Renal, Urinary & Pathology (Path) 8
glomerulonephritis glomeruli. IF demonstrates a 'lumpy-bumpy' granular deposits of IgG and C3 on the GBM, and subepithelial, electron-dense deposits are seen on EM. Electrolytes (RE)
12 Poststreptococcal PSGN is the most common cause of nephritic syndrome in children. LM demonstrates enlarged, hypercellular glomeruli. Lab findings in PSGN incl ↑ anti-streptococcal Renal, Urinary & Pathology (Path) 8
glomerulonephritis Abs (e.g. ASO, anti-DNase B) and ↓ C3 and total complement lvls. C4 lvls are usually normal. Electrolytes (RE)
13 Granulomatosis with Pauci-immune rapidly progressive glomerulonephritis frequently occurs as a manifestation of antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitides (eg, Renal, Urinary & Pathology (Path) 2
polyangiitis granulomatosis with polyangiitis, microscopic polyangiitis). It is characterized by glomerular crescent formation without immunoglobulin or complement deposits. Electrolytes (RE)
14 Hydrocephalus Hydrocephalus is an enlargement of the ventricles (+/- ↑ pressure) caused by either neuronal volume loss (eg, hydrocephalus ex-vacuo) or excessive CSF accumulation Nervous (NS) Pathology (Path) 4
(due to flow obstruction or impaired absorption). Neurodegenerative diseases (eg, AIDS dementia) can be a/w hydrocephalus ex-vacuo due to significant cortical atrophy,
which allows the ventricles to expand while maintaining normal pressure.
15 Hydrocephalus Symmetrical enlargement of the ventriculi is Chx of communicating hydrocephalus. Communicating hydrocephalus usually occurs 2° to dysfxn or obliteration of Nervous (NS) Pathology (Path) 4
subarachnoid villi. This dysfxn is usually a sequelae of meningeal infection (including tuberculosis meningitis) or SAH/IVH.
16 Normal pressure NPH presents w/ progr gait difficulties, cognitive disturbances, and urinary incontinence. It's a form of communicating hydrocephalus characterised by ventriculomegaly Nervous (NS) Pathology (Path) 2
hydrocephalus w/o persistent ↑ in ICP. Brain imaging reveals ventricular enlargement out of proportion to sulci enlargement.
17 Normal pressure NPH occurs due to ↓ CSF absorption, resulting in ventriculomegaly w/ normal ICP. This causes stretching of the descending cortical fibers (corona radiata) from the Nervous (NS) Pathology (Path) 2
hydrocephalus frontal lobe and contributes to the classic triad of SSx (ie, dementia, gait abnormalities, urinary incontinence). Loss of cortical inhibition of the sacral micturition center
leads to urge incontinence.
18 Ischemic stroke Global cerebral ischemia is typically precipitated by systemic hypotension (e.g. cardiac arrest). The cells most susceptible to ischemia are the CA1 pyramidal neurons of Nervous (NS) Pathology (Path) 19
the hippocampus. Other areas of the brain that are damaged early in the course of global cerebral ischemia incl the cerebellar Purkinje cells and the pyramidal neurons of
the neocortex.
19 Ischemic stroke Inadequate blood supply to the brain (e.g. arterial thrombosis or embolism) leads to ischemic stroke. The 1st microscopic changes are typically seen 12-24hrs after Nervous (NS) Pathology (Path) 19
irreversible ischemic injury and incl intense eosinophilic staining of the neuronal cytoplasm (red neurons) and nuclear fragmentation.
20 Ischemic stroke Microglia are the predominant cell in the necrotic area 3-7 days after the onset of ischemia and phagocytize the fragments of neurons, myelin, and necrotic debris. Nervous (NS) Pathology (Path) 19
21 Ischemic stroke Occlusion of the MCA typically results in contralateral hemiparesis and hemisensory loss of the face and upper limb w/ relative preservation of lower limb fxn. If the Nervous (NS) Anatomy (Anat) 19
occluded MCA is in the dom (usually left) hemisphere, aphasia may also occur.
22 Ischemic stroke Lacunar infarcts are small ischemic infarcts (<15mm in diameter) involving the deep brain structures (e.g. basal ganglia, pons) and subcortical white matter (e.g. internal Nervous (NS) Pathology (Path) 19
capsule, corona radiata). They're most often due to lipohyalinosis, microatheroma formation, and hardening/thickening of the vessel wall (HTN arteriolar sclerosis), which
predisposes to thrombotic vessel occlusion.
,QID Topic Educational Objective System Subject Repeats
23 Ischemic stroke Sustained cerebral hypoperfusion (eg, hypotension, shock) may cause global cerebral ischemia and watershed infarction. These watershed zones are located at the borders Nervous (NS) Pathology (Path) 19
b/w areas perfused by the ACAs, MCAs, and PCAs and typically appear as symmetric, bilateral wedge-shaped strips of necrosis over the cerebral convexity, parallel and
adjacent to the interhemispheric fissure.
24 Glomerular disorders Crescent formation on LM is Dx for RPGN. Crescents consist of glomerular parietal cells, lymphocytes, and macrophages along w/ abundant fibrin deposition. Crescents Renal, Urinary & Pathology (Path) 9
eventually become fibrotic, disrupting glomerular fxn and causing irreversible renal injury. Electrolytes (RE)
25 Poststreptococcal PSGN presents w/ oedema, HTN, and hematuria after a streptococcal infection. Most children recover completely, but adult pts have a relatively poor prognosis and Renal, Urinary & Pathology (Path) 8
glomerulonephritis higher risk of chronic HTN and renal insufficiency. Electrolytes (RE)
26 Renal vein thrombosis Nephrotic syndrome is a hypercoagulable state. Sudden-onset abdominal or flank pain, hematuria, and left-sided varicoceles suggest RVT, a well-known complication of Hematology & Pathology (Path) 1
nephrotic syndrome. Loss of anticoagulant factors, especially AT-III, is responsible for the thrombotic and TE complications of nephrotic syndrome. Oncology (HO)
27 Poststreptococcal Poststreptococcal glomerulonephritis is an immune complex-mediated disease that occurs 2-4 weeks after group A β-hemolytic Streptococcus infection. Immune Renal, Urinary & Histology (Hist) 8
glomerulonephritis complexes composed of IgG, IgM, and C3 are deposited along the glomerular basement membrane and are visible on electron microscopy as large, dome-shaped, Electrolytes (RE)
subepithelial, electron-dense deposits.
28 Glomerular disorders MCD is the most common childhood nephrotic syndrome. ↑ glomerular cap permeability causes massive protein (e.g. albumin) loss in the urine. Hypoalbuminaemia ↓ Renal, Urinary & Pathology (Path) 9
plasma oncotic pressure, which causes a fluid shift into the interstitial space, resulting in oedema. Low oncotic pressure also triggers ↑ LP production in the liver (i.e. Electrolytes (RE)
hyperlipidaemia).
30 Turner syndrome Aortic coarctation in a child/young adult presents with lower-extremity claudication (eg, pain and cramping with exercise), blood pressure discrepancy between the upper Cardiovascular (CV) Genetics (Gene) 8
and lower extremities, and delayed or diminished femoral pulses. Turner syndrome (45,XO) is associated with coarctation of the aorta in up to 10% of cases.
31 Aortic coarctation Pts w/ adult-type coarctation of the aorta commonly die of HTN-assoc complications, incl LV failure, ruptured dissecting AA, and SICH. These pts are at ↑ risk for Cardiovascular (CV) Pathology (Path) 1
ruptured intracranial aneurysms b/c of the ↑ incidence of congenital BAs of the COW as well as aortic arch HTN.
32 Patent ductus arteriosus Digital clubbing and cyanosis w/o BP or pulse discrepancy are pathognomonic for a large PDA complicated by Eisenmenger syndrome (reversal of shunt flow from L-R Cardiovascular (CV) Pathology (Path) 4
to R-L). Severe coarctation of the aorta can cause lower extremity cyanosis. R-L shunting in pts w/ large septal defects and TOF results in whole-body cyanosis.
33 Bicuspid aortic valve AS is the most common complication of bicuspid AVs. Pts w/ bicuspid AVs develop clinically significant AS on average around age 50. In comparison, senile calcific Cardiovascular (CV) Pathophysiology 1
stenosis of normal AVs generally becomes SSx age >65. (Patp)
34 DiGeorge syndrome Chromosome 22q11.2 microdeletion results in DGS (cardiac anomalies, hypoplastic or absent thymus, and hypocalcemia) and VCFS (cleft palate, cardiac anomalies, Miscellaneous Genetics (Gene) 2
dysmorphic facies). FISH is the "gold standard" for detecting a microdeletion. (Multisystem) (MS)
35 Transposition of the great An echocardiogram showing an aorta lying anterior to the pulmonary artery is diagnostic of transposition of the great arteries (TGA). This life-threatening cyanotic Cardiovascular (CV) Embryology 1
vessels condition results from failure of the fetal aorticopulmonary septum to spiral normally during septation of the truncus arteriosus. (Embr)
36 Atherosclerosis Stable angina pectoris results from myocardial O2 demand-supply mismatch and MFx as chest pressure, tightness, or pain that is reliably produced by exertion and Cardiovascular (CV) Pathology (Path) 8
relieved by rest. It most commonly occurs due to a fixed atherosclerotic plaque obstructing >70% of the coronary artery lumen that limits blood flow during exertion.
37 Myocardial infarction STEMI involves transmural (full-thickness) infarction of the myocardial wall, and usually results from acute atherosclerotic plaque rupture w/ the devel of overlying Cardiovascular (CV) Pathology (Path) 18
thrombus that fully occludes the coronary artery lumen. It classically presents w/ sudden-onset substernal chest pain that's not relieved by rest or short-acting nitrates.
ECG demonstrates STE in the affected leads w/ subseq devel of Q waves.
39 Vasospastic angina Prinzmetal (variant) angina is Chx by episodic, transient atks of coronary vasospasm (at rest and at night), producing temporary transmural myocardial ischemia w/ ST- Cardiovascular (CV) Pathology (Path) 2
segment elevation. Possible triggers are cigarette smoking, cocaine/amphetamines, and dihydroergotamine/triptans. Tx includes tobacco/Rx cessation and vasodilator Thx
(eg, nitrates, CCBs).
40 Atherosclerosis Gradually developing myocardial ischemia encourages the formation and maturation of collateral vessels and is most likely to occur in the setting of a slow-growing, Cardiovascular (CV) Pathology (Path) 8
stable atherosclerotic plaque. An unstable atherosclerotic plaque (eg, that w/ active inflammation, a lipid-rich core, a/o a thin fibrous cap) is more likely to rupture,
resulting in the abrupt onset of ischemia/infarction that precludes the development of viable collateral vessels.
42 Myocardial infarction After the onset of severe ischemia leading to MI, early signs of coag necrosis don't become apparent on LM until 4hrs after the onset of MI. Cardiovascular (CV) Pathophysiology 18
(Patp)
43 Myocardial infarction Loss of cardiomyocyte contractility occurs w/i 60 2nds after the onset of total ischemia. When ischemia lasts less than 30 min, restoration of blood flow leads to reversible Cardiovascular (CV) Pathology (Path) 18
contractile dysfxn (myocardial stunning), w/ contractility gradually returning to normal over the next several hrs to days. However, after about 30 min of total ischemia,
ischemic injury becomes irreversible.
44 Myocardial infarction Hibernating myocardium refers to the presence of LV systolic dysfxn due to ↓ coronary blood flow at rest that's partially or completely reversible by coronary Infectious Diseases Microbiology 18
revascularisation. (ID) (Micr)
45 Hepatitis C Genetic variations created during HCV replication result in marked variety in the Agic structure of HCV envelope proteins. The production of host Abs lags behind that of Infectious Diseases Microbiology 4
new mutant HCV strains, preventing infected individuals from mounting an effective immune response. (ID) (Micr)
,QID Topic Educational Objective System Subject Repeats
46 Hepatitis D HDV is a replication-defective RNA virus that's capable of causing infection only in the setting of coinfection w/ HBV. HBV provides HBsAg for the HDV envelope. Infectious Diseases Microbiology 2
(ID) (Micr)
47 Hepatitis B Infants born to HBeAg-positive mothers have a high risk of acquiring perinatal hepatitis B virus (HBV) infection. Infected neonates have high levels of HBV replication Gastrointestinal & Microbiology 14
and are at high risk for chronic infection, but are usually asymptomatic or have only mildly elevated liver function tests. Nutrition (GI) (Micr)
48 Hepatitis D The HBsAg of HBV must coat the HDAg of HDV before it can infect hepatocytes and multiply. Infectious Diseases Microbiology 2
(ID) (Micr)
54 Hepatitis E HEV is an unenveloped, ssRNA virus spread thru the faecal-oral route. The most concerning feature of hepE infection is the high mortality rate observed in infected preg Gastrointestinal & Pathology (Path) 1
women Nutrition (GI)
56 Hemangioma Cavernous hemangioma is the most common benign liver tumour. Microscopically, these tumours consist of cavernous, blood-filled vascular spaces of variable size lined Gastrointestinal & Pathology (Path) 6
by a single epithelial layer. The Bx of a suspected hemangioma is not advisable, as the procedure has been known to cause fatal hemorrhage and is of low Dx yield. Nutrition (GI)
57 Hepatocellular cancer AFP is a serum tumour marker that's often moderately ↑ in pts w/ chronic viral hepatitis. However, it can be strikingly ↑ in those w/ HCC, and a sudden rise can be a sign Gastrointestinal & Pathology (Path) 5
that a pt w/ chronic liver disease is harbouring HCC. Nutrition (GI)
58 Hepatocellular cancer High lvls of dietary aflatoxin exposure is a/w a G:C → T:A transversion in codon 249 of the p53 gene, a mut thought to greatly ↑ the risk of devel HCC. Hematology & Pathology (Path) 5
Oncology (HO)
59 Hepatocellular carcinoma Both HBV and HCV infections ↑ the risk of HCC due to chronic hepatic inflammation and cell turnover. HBV is also carcinogenic due to the production of oncogenic Gastrointestinal & Pathology (Path) 1
proteins and the insertion of the HBV genome into the host chrom. Nutrition (GI)
60 Metastatic liver disease Malignant hepatic lesions most often represent mets from another 1° site (e.g. breast, lung, colon); 1° liver neoplasms (e.g. HCC) are much less common. Infectious Diseases Pathology (Path) 1
(ID)
61 Hepatocellular cancer Universal vaccination of children against HBV would likely cause a steep decline in the worldwide incidence of hepatocellular carcinoma. Infectious Diseases Pathophysiology 5
(ID) (Patp)
62 Echinococcosis Echinococcus granulosus is the most common cause of hydatid cysts. Spilling of cyst contents can cause anaphylactic shock. Surgical manipulation should be performed Gastrointestinal & Microbiology 1
with caution. Nutrition (GI) (Micr)
63 Liver abscess S. aureus can cause hepatic abscesses via heme seeding of the liver. Enteric bacteria (e.g. E. coli, Klebsiella, and enterococci) can cause hepatic abscesses by asc the Nervous (NS) Pathology (Path) 1
biliary tract (i.e. asc cholangitis), portal vein pyemia, or direct invasion from an adjacent area (e.g. cholecystitis).
64 Wernicke-Korsakoff Oculomotor dysfxn, ataxia, and confusion form the triad of WE. Most of these SSx usually resolve after vitB1 administration. Korsakoff syndrome is a complication of Nervous (NS) Biochemistry 5
syndrome WE, the hallmarks of which are permanent memory loss and confabulation. (Bioc)
65 Vitamin B12 deficiency Vit B12 defx often Px w/ megaloblastic anemia (impaired DNA synthesis) and neuro deficits (impaired myelin synthesis). Chx neuro findings include SCD of the dorsal Nervous (NS) Pathology (Path) 9
columns and lateral corticospinal tract. ↑ in methylmalonic acid and homocysteine lvls occur due to ↓ metabolism of these molecules.
66 Vitamin B12 deficiency Myelopathy a/w vitB12 defic is called SCD. 'combo' refers to myelin degen of both the ascending (dorsal columns) and descending (corticospinal tract) pathways. Loss of Nervous (NS) Pathology (Path) 9
position and vibration sensation, sensory ataxia, and spastic paresis are common MFxs.
67 Guillain-Barre syndrome GBS is an acute, demyelinating polyneuropathy thought to be caused by molecular mimicry. Abs formed against infectious agents cross-react w/ myelin and Schwann Gastrointestinal & Biochemistry 3
cells, leading to immune-mediated demyelination. LM shows segmental demyelination and an endoneurial inflammatory infiltrate composed of lymphocytes and Nutrition (GI) (Bioc)
macrophages.
68 Gallstone disease Fibrate Rx (e.g. fenofibrate, gemfibrozil) inhib cholesterol 7α-hydroxylase, which catalyzes the RLS in the synthesis of BAs. The ↓ BA production results in ↓ cholesterol Pregnancy, Childbirth Pathophysiology 8
solubility in bile and favors the formation of cholesterol gallstones. & Puerperium (PR) (Patp)
69 Gallstones and pregnancy Estrogen-induced cholesterol hypersecretion and progesterone-induced gallbladder hypomotility are responsible for the ↑ incidence of cholelithiasis in women who are Hematology & Pathology (Path) 1
pregnant or using oral contraceptives. Oncology (HO)
70 Gallstone disease Black pigment stones arise from conditions that ↑ the amount of unconjugated bilirubin in bile, which promotes Ca2+ bilirubinate precipitation. This may occur in the Gastrointestinal & Biochemistry 8
setting of chronic hemolysis (e.g. SCA, β-thalassaemia, HS) and ↑ enterohepatic cycling of bilirubin (e.g. ileal disease). Nutrition (GI) (Bioc)
71 Gallstone disease Brown pigment gallstones are composed of Ca salts of unconjugated bilirubin and arise 2° to bacterial or helminthic infection of the biliary tract. β-glucuronidase released Gastrointestinal & Pathology (Path) 8
by injured hepatocytes and bacteria hydrolyzes bilirubin glucuronides to unconjugated bilirubin. The liver fluke Clonorchis sinensis has a high prevalence in East Asian Nutrition (GI)
countries and is a common cause of pigment stones.
72 Gallstone disease The gallbladder fxns to actively absorb water from bile. Gallbladder hypomotility causes the bile to become concentrated, promoting precipitation and accumulation of Cardiovascular (CV) Pathology (Path) 8
particulate material. This forms a viscous biliary sludge that can cause transient BDO (biliary colic) and promote cholesterol gallstone formation.
73 Endocarditis Janeway lesions are nontender, macular, and erythematous lesions typically located on the palms and soles of pts w/ acute IE and are the result of septic embolization from Cardiovascular (CV) Pathology (Path) 15
valvular vegetations.
, QID Topic Educational Objective System Subject Repeats
74 SLE CV MFx of lupus include accelerated atherosclerosis, small-vessel necrotizing vasculitis, pericarditis, and Libman-Sacks endocarditis (small, sterile vegetations on both Cardiovascular (CV) Pathology (Path) 7
sides of the valve). Renal involvement classically MFx as DPGN, which is Chx by diffuse thickening of the glomerular capillary walls w/ "wire-loop" structures on LM.
75 Carcinoid tumors Carcinoid syndrome typically presents w/ episodic flushing, secretory diarrhoea, and wheezing. It can lead to pathognomonic plaque-like deposits of fibrous tissue on the Cardiovascular (CV) Pathophysiology 4
right-sided endocardium, causing TR and right-sided HF. ↑ 24-hr urinary 5-HIAA can confirm the Dx. (Patp)
76 Dilated cardiomyopathy DCM results from direct dmg to cardiomyocytes leading to myocardial contractile dysfxn (systolic dysfxn), volume overload, and ventricular dilation. Viral myocarditis is Cardiovascular (CV) Pathology (Path) 8
a common cause of DCM and should be suspected in young pts who develop HF following a SSx viral prodrome.
77 Hypertrophic In pts w/ HCM, dynamic LVOT obstr is due to abn systolic anterior motion of the anterior leaflet of the MV toward a hypertrophied IV septum. Gastrointestinal & Pathophysiology 9
cardiomyopathy Nutrition (GI) (Patp)
78 Gallstone disease The absence of normal enteral stim in pts receiving TPN leads to ↓ CCK release, biliary stasis, and ↑ risk of gallstones. Resection of the ileum can also ↑ the risk of Gastrointestinal & Pathophysiology 8
gallstones due to disruption of normal enterohepatic circulation of the BAs. Nutrition (GI) (Patp)
79 Gallstone disease ↑ chol concs ↑ the likelihood of chol precipitation and gallstone formation. High lvls of bile salts and PC ↑ chol solubility and ↓ the risk of gallstones. Gastrointestinal & Pathology (Path) 8
Nutrition (GI)
80 Cholecystitis Acute calculous cholecystitis is an acute inflammation of the gallbladder initiated by gallstone obstruction of the cystic duct. Subsequent steps in pathogenesis include Gastrointestinal & Pathophysiology 5
mucosal disruption by lysolecithins, bile salt irritation of the luminal epithelium, PG release w/ transmural inflammation, gallbladder hypomotility, ↑ intraluminal pressure Nutrition (GI) (Patp)
causing ischemia, and bacterial invasion.
81 Cholecystitis Acute cholecystitis is most often caused by gallstones obstructing the cystic duct. The diagnosis can be made by identifying signs of gallbladder inflammation (eg, wall Gastrointestinal & Pathology (Path) 5
thickening, pericholecystic fluid) on ultrasonography. When ultrasound is inconclusive, nuclear medicine hepatobiliary scanning (ie, cholescintigraphy) can be used to Nutrition (GI)
assess cystic duct patency and make the diagnosis.
82 Cholecystitis Acute acalculous cholecystitis is an acute inflammation of the gallbladder in the absence of gallstones. It typically occurs in critically ill pts (eg, those w/ sepsis, severe Cardiovascular (CV) Pathology (Path) 5
burns, trauma, immunosuppression) due to gallbladder stasis and ischemia. CFx may be subtle and include fever, RUQ pain, and leukocytosis.
83 Hypertrophic HCM is a common cause of SCD in young adults. Histologic features incl cardiomyocyte hypertrophy and myofiber disarray w/ ↑ interstitial fibrosis. The structural Cardiovascular (CV) Pathology (Path) 9
cardiomyopathy disarray creates a substrate for ventricular arrhythmia (e.g. v-tach, VF) that can lead to SCD.
84 Hypertrophic HCM is Chx by asymmetric (eg, septal) LVH that can result in SCD. AD mutations affecting the cardiac sarcomere genes (eg, cardiac β-myosin heavy chain gene and Cardiovascular (CV) Pathology (Path) 9
cardiomyopathy myosin-binding protein C gene) are responsible for the majority of cases.
85 Long QT syndrome Unprovoked syncope in a previously aSSx young person may result from a congenital LQTS. The 2 most important congenital syndromes w/ QT prolongation — RWS Cardiovascular (CV) Pathophysiology 4
and JLNS — are thought to result from muts in a K+ channel protein that contributes to the delayed rectifier current (IK) of the cardiac AP. (Patp)
86 Hypertrophic HCM is characterised by asymmetric ventricular septal hypertrophy and dynamic LVOT obstr. ↓ in LV blood volume, via manoeuvres or conditions that ↓ preload (e.g. Cardiovascular (CV) Pathology (Path) 9
cardiomyopathy abrupt standing, Valsalva strain phase) or afterload, worsen LVOT obstr and ↑ the intensity of the HCM murmur.
87 Long QT syndrome Congenital LQTS is most often caused by genetic muts in a K+ channel protein that contributes to the outward-rectifying K+ current. A ↓ in the outward K+ current leads Gastrointestinal & Pathology (Path) 4
to prolongation of AP duration and QT interval. This prolongation predisposes to the devel of life-threatening ventricular arrhythmias (e.g. TdP) that can cause Nutrition (GI)
palpitations, syncope, seizures, or SCD.
88 Porcelain gallbladder Porcelain gallbladder is a potential MFx of chronic cholecystitis and is often found in a/w multi gallstones. It's due to dystrophic intramural deposition of Ca2+ salts in the Gastrointestinal & Pathology (Path) 1
setting of chronic inflammation. Porcelain gallbladder is a/w an ↑ risk of adenocarcinoma of the gallbladder. Nutrition (GI)
89 Bowel obstruction Gallstone ileus is a mech bowel obstr caused when a large gallstone erodes into the intestinal lumen. Pneumobilia (air in the biliary tract) is a common finding. Cardiovascular (CV) Pathology (Path) 1
90 Acute pericarditis In contrast to angina, the chest pain of pericarditis is sharp and pleuritic and may be exacerbated by swallowing or coughing. PIP occurs b/w 2 and 4 days following a Cardiovascular (CV) Pathophysiology 5
transmural MI. PIP is an inflammatory rxn to cardiac muscle necrosis that occurs in the adjacent pericardium. (Patp)
91 Wolff-Parkinson-White Wolff-Parkinson-White syndrome is characterized by symptomatic paroxysmal supraventricular tachycardia (eg, atrioventricular reentrant tachycardia) due to the Cardiovascular (CV) Pathology (Path) 2
syndrome presence of an accessory conduction pathway. During normal sinus rhythm, the presence of this accessory pathway causes ventricular preexcitation, which can be
identified on ECG by the triad of a shortened PR interval, early upslope of the QRS complex (delta Wave), and a widened QRS interval.
92 Long QT syndrome Jervell and Lange-Nielsen syndrome is an AR disorder Chx by profound bilateral sensorineural hearing loss and congenital LQTS, which predisposes to ventricular Cardiovascular (CV) Pathology (Path) 4
arrhythmias and SCD. This condition occurs 2° to mutations in genes that encode voltage-gated K channels.
93 Dilated cardiomyopathy Dilation of the LV cavity commonly occurs in response to systolic dysfxn (eg, ischemic heart disease, DCM) or certain types of valvular disease (ie, AR, MR). Chronic Cardiovascular (CV) Pathophysiology 8
volume overload causes progressive eccentric hypertrophy that eventually leads to ↓ ventricular contractility and DHF. (Patp)
94 Restrictive cardiomyopathy Diastolic HF is caused by ↓ ventricular compliance and is characterised by normal LV EF, normal LV EDV, and ↑ LV filling pressures. HTN, obesity, and infiltrative Cardiovascular (CV) Pathology (Path) 1
disorders (e.g. transthyretin-related amyloidosis, sarcoidosis) are important causes of DHF.
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