Step Flashcards
Most reliable ausculatory finding indicating mitral stenosis severity
A2-OS interval. As the pressure increases it becomes more difficult to push blood out of the LA, so the OS occurs sooner to provide more time to generate the pressure.
Chemoprophylaxis for meningococcal disease, Mechanism
1) Rifampin -penetrates well into all tissues. Inhibits DNA dependent RNA polymerase
2) Ciprofloxacin -risk of CT pathology
3) IM ceftriaxone -pnful route
4) sulfamethoxazole- Resistance
Bounding femoral and carotid pulses w/ head bobbing
Early blowing, diastolic decrescendo murmur best at left 3 or 4 ICS
Aortic Regurgitation
Wide pulse pressure (water-hammer)
Stroke volume increases due to increased preload, when the LV relaxes during diastole blood flows backwards and out of the arteries (collapsing arteries)
Lithium interaction with a hypertensive med leading to nonspecific T wave abnormalities
Hydrochlorothiazide
Volume depletion leads to increased reabsorption of Lithium in the PCT.
Chronic Lithium toxicity DDI
(volume depletion) Thiazides, ACEI, and NSAIDS
confusion, ataxia, neuromuscular excitability
Hyperosmotic volume contraction
osmol increase, ECF decreased, ICF decreased
Diabetes insipidus or decreased fluid intake, increased sweating
Central DI
Decreased ADH released -> water is not reabsorbed and the urine is very dilute
Isosmotic volume contraction
osmol same, ECF decreased, ICF same
osmol same, ECF decreased, ICF same
Acute GI hemorrhage or diarrhea -fluid is only lost from the ECF (blood vessels)
Hyposmotic volume contraction
osmol decreased, ECF decreased, ICF increased
Adrenal insufficency - lack of aldosterone
NaCl not reabsorbed-> ECF decreased.
ECF is low on solutes, so water shifts into cells (ICF)
Hypertonic volume expansion
osmol increased, ECF increased, ICF decreased
Hypertonic saline infusion- ECF volume and osmolarity increase
Water leaves the ICF to dilute the ECF
Hyposmotic volume expansion
osmol decrease, ICF increase, ECF same
Primary polydipsia and SIADH
Increased water intake or reabsorption shifts into ICF to dilute with the ECF staying the same. The increased water leads to overall decreased osmolarity
Onion-like concentric thickening of arteriolar walls
Hyperplastic arteriolosclerosis
Malignant HTN pathology
Homogenous acellular thickening of arteriolar walls
Hyaline arteriosclerosis
Lower HTN
Granulomatous inflammation of the media
Giant cell arteritis
Transmural inflammation of the arterial wall w/ fibrinoid necrosis
Polyarteritis nodosa
Smooth transition for impatient to outpatient
Discharge checklist
Down Syndrome Fetal Markers
AFP low
B-Hcg high
Inhibin A high
Chediak Higashi: What is it? Signs
Microtubule Disorder of neutrophil phagolysosome fusion
Partial albinism, peripheral neuropathy, recurrent pyogenic infxns
Proximal muscle weakness and Gottron’s papules (ertythematous plaques over hand joints)
Dermatomyositis
Dermatomyositis association
Often paraneoplastic to lung, colorectal, and ovarian CA
Blistering cutaneous photosensitivity
Uroporphorinogen decarboxylase deficency
Porphyria cutaenous tardia
Paraventricular tumor
Perivascular rosettes
Ependymoma
Cerebral hemisphere tumor
Hypercellular areas of atypical astrocytes bordering regions of necrosis (pseudopalisading)
Glioblastoma
Cerebellar tumor in kids
Small blue cells surrounding a neurophil
Homer-Wright Rosettes
Medulloblastoma
White matter of cerebral hemispheres
Round nuclei w/ halo of clear cytoplasm (Fried egg cells)
Oligodendroglioma
Cerebellar tumor in kids
eosinophilic granular bodies and elongated hairlike fibers (Rosenthal fibers)
Pilocytic astroocytoma
Spindle cells w/ palisading nuclei arranged around Verocay bodies composed of eosinophilic cores (antoni A)
Cerebelloponite angle
Schwannoma
Benign suprasellar tumor in kids
cords/nests of palisading squamous epithelium w/ internal areas of lamellar “wet keratin”
Adamantinomatous craniopharyngioma
Moldy grains in China w/ substance causing G to T mutation in p53 increase risk of what cancer?
Aflatoxins from aspergillus -> increased risk of HCC
Lac P
Promoter region where RNA polymerase binds
Lac I
gene for repressor -binds operator to prevent RNA polymerase binding. Constitutively on
Lac O
Operator- where the repressor binds, downstream of promoter region
Lactose (inducer)
Binds to the repressor to prevent it from binding to the operator and preventing RNA polymerase
Lac operon regulation
1) negative - repressor binds to operator preventing RNA polymerase from binding the promoter
2) cAMP-CAP binding upstream from the promoter. High glucose-> decreased cAMP.
Low glucose-> high cAMP-> binding to CAP-> cAMP-CAP binding to promoter
Patient is using herbal supplements that have not caused them SE
Advise on safety, quality, and efficacy
Conduct Disorder vs. Antisocial personality disorder
Conduct before 18, antisocial after 18
Persistent pattern of violating societal norms and other’s rights
Ligated IMA, which artery provides collateral circulation to the descending colon (not rectum)
SMA via marginal artery of Drummond
AIDS pt w/ working memory problem, executive dysfxn, and slow information processing
HIV associated dementia
HIV associated dementia histology
Microglial nodules, groups of activating macrophages and microglial cells around small areas of necrosis. They may fuse to form multinucleated giant cells
Mycobacterial Drug resistance due to non-expression of catalase-peroxidase enzyme
Resistance to INH. INH must be processed by mycobacterial catalase-peroxidase to be activated
Post-streptococcal glomerulonephritis complication risk increases for which pts?
Adults have poor prognosis due to higher risk of chronic HTN and renal insufficiency
Enzyme deficiencies of early steps in porphyrin synthesis
Neuropsych w/o photosensitivity due to metabolite accumulation
Uroporphyrinogen decarboxylase deficiency
Vesicles and blisters on sun exposed areas, edema, pruritus, pain, and erythema
Inflammatory arthritis, ulcer of the hard palate, butterfly rash
SLE-
ANA, anti-smith (spliceosome snRNP), anti-dsDNA
ALS microscopic
Loss of anterior horn - LMN lesions - muscle weakness and atrophy
Demyelnation of lateral corticospinal tracts - UMN lesion -spasticity and hyperreflexia
Can affect CN 5,9,10,12
ALS mutation
SOD1 -gene that codes for copper-zinc superoxide dismutase
Synovial WBC >100,000 and no crystals
Septic arthritis Tx w/ abx to prevent joint destruction, osteomyelitis, and sepsis
Acutr tx of gout when pt has peptic ulcer dz
Colchicine
Colchicine mechanism
Binds to intracellular tubulin and inhibits MT polymerizaton. Disrupts chemotaxis and phagocytosis
Colchicine SE
diarrhea, nausea, abd pn
Primary biliary cirrhosis classic pt
Pruritus and fatigue in middle aged woman
Cholestasis - jaundice, pale stool, dark urine
hypercholesterolemia - xanthelesmas
What does spironolactone due with K and H
Spironolactone blocks Na reabsorption and increases K and H reabsorption.
Fewer hydrogen ions are secreted from the collecting tubules
PCT osmolarity
300 isotonic w/ plasma regardless of final urine concentration
Descending loop of Henle osmolarity
Water leaves the tubule and the filtrate becomes concentrated, >300. ADH is high it will =1200
Ascending loop of henle osmolarity
Water comes back in to dilute the filtrate. <300
Distal convoluted tubule osmolarity
Most dilute section, impermeable to water, 100 osmol
Collecting duct osmolarity
Water leaves the tubule to dilute the hypertonic interstitium. So the somolarity is around 1200
Thyroid cytology - clusters of overlapping cells w/ large nuclei containing sparse, finely dispersed chromatin
Intranuclear inclusion bodies and grooves
Thyroid papillary carcinoma
Ground glass -Orphan Annie eyes
Psammoma bodies
Thyroid cytology - markedly pleomorphic cells, including irregular giant cells and biphasic spindle cells
Anaplastic cancer
Thyroid cytology - colloid nodule
Benign hyperplasia
Thyroid histology- Polygonal to spindle shaped cells w/ slightly granular cytoplasm.
Stains for calcitonin.
Adjacent amyloid deposits
Medullary thyroid cancer - from parafollicular C cells
MEN 2A and 2B
Homeless male w/ abd pn,
Develops acute confusion, nystagmus and b/l abducens palsy
b/l lesions in the mamillary body and Periaqueductal gray matter in the hospital
Wernicke’s encephalopathy triad - ataxia, ophthalmoplegia, confusion
Thiamine deficient pt given glucose
Develop Wernicke encephalopathy -added glucose worsens thiamine deficiency. Thiamine is cofactor for glucose metabolism (decarboxylase rxns)
Car accident pt develops excessive thirst and frequent urination that continues weeks later
Central DI - hypothalmic nuclei injury. Posterior pituitary injury would be transient
How is INH metabolized?
Acetylation to N-acetyl-INH
Bimodal distribution of metabolism
Fast and slow acetylators
Large mass surrounding the intestines
Uniform, round, medium-sized tumor cells w/ basophilic cytoplasm and proliferation fraction (Ki-67 fraction) of >99%
EBV - Burkitt Lymphoma (starry sky)
Chronic non-atrophic gastritis affecting the antrum: cause
H. Pylori infxn
Atrophic chronic gastritis of the body
Pernicious anemia
Most common benign liver tumor
Cavernous hemangioma - cavernous blood filled vascular spaces lined by a single epithelial layer
Which liver tumor can regress w/ d/c OC
hepatic adenoma
NOD2 mutation -> NF -KB decrease. What will be impaired
Cytokine production will be impaired -> impaired innate barrier fxn
Bugs get in and cause exagerated immune response
Fever, neuro sx (progressive lethargy), renal failure, anemia, and thrombocytopenia in setting of GI illness
Classic pentad of thrombocytopenic thrombotic purpura
Plt activation in arterioles and capillaries
Diffuse microvascular thrombosis
Microangiopathic hemolytic anemia w/ schistocytes
Thrombocytopenia
Clinical and pathologic features of thromobocytopenic thrombotic purpura
S-shaped bacteria causes decreased somatostatin-producing antral cells, what will this lead to
Duodenal ulcer as decreased somatostatin will lead to decreased inhibition of gastrin. The loss of somatostatin does not lead to gastric lymphoma, even though MALTs are possible with prolonged infxn
s/p coronary artery stent, livedo reticularis, hx of hyperlipidemia and CAD. What does biopsy of the kidney look like?
Cholesterol clefts in the arterial lumen. Cholesterol debris gets lodged leaving needle shaped clefts in intralobular renal arteries
Polycystic kidney dz w/ bone pn and weakness - Levels of Phosphate, PTH, and Calcitriol
-Phosphate is increased due to decreased GFR (less phosphorus filtered)
-Calcitriol is decreased, Hyperphosphatemia stims osteoclasts to secrete FGF, which is meant to decrease Phosphate reabsorption, but also decreases calcitriol synthesis
PTH is increase due to low Ca and high phosphate
Pulmonary histology - columnar mucin secreting cells that line the alveolar spaces w/o invading the stroma. How would you classify?
Malignant neoplasm, adenocarcinoma in situ (formerly bronchioalveolar carcinoma)
Why does a rt mainstem bronchus obstruction present as a u/l completely opacified lung
All of the alveoli collapse (atelectasis) - there is no air in the lung. It condenses into what looks like a solid organ.
Why is pancreatitis a risk factor for ARDS?
Pancreatitis leads to release of inflammatory cytokines and pancreatic enzymes that lead to neutrophils attacking the pulmonary interstitium and alveoli
ARDS Pathology
interstitial and alveolar edema, inflammation, and fibrin deposition cause the alveoli to become lined with waxy hyaline membranes
ARDS impact on the lungs: capillary permeability, lung compliance, WOB, V/Q match, PCWP
Decreased capillary permeability-> edema and decrease lung compliance, increased WOB, and atelectasis->V/Q mismatch, not ventilated, but perfused (shunt)
PCWP is NL
Why is Pulmonary capillary wedge pressure NL in ARDS
Noncardiogenic pulmonary edema
The problem is in the lungs not the heart, so the LA pressure is NL
Bright red hematemesis, splenomegaly, no liver biopsy abnormalities
Hepatic vein thrombosis - The obstruction is before the liver, so it is not affected. Blood spills back into anastamoses w/ systemic circulation
Budd-Chiari liver biopsy
Occlusion of hepatic vein leaving the liver. Centrilobular congestion and fibrosis
Porcelain gallbladder pathology
Chronic cholecystitis. Dystrophic intramural deposition of Ca salts.
Porcelain gallbladder increases risk of what?
Galbladder adenocarcinoma
Anti- tissue transglutaminase, where do you biopsy to confirm dx?
Celiac dz, biopsy the duodenum.
Duodenum and jejunum see highest level of gliadin
Crohn dz, where do you biopsy?
terminal ileum
Ischemia induced ventricular arrhythmias, tx w/?
Class IB antiarrhythmics,
mexiletine
lidocaine
Weakest Na channel blocker, dissociates the fastest, small effect on QRS, prefer inactivated channels
Class IB antiarrhythmics
mexiletine
lidocaine
Hypotension baroreceptor response
Low BP -> decreased stretch -> decreased baroreceptor signal -> increased SNS stimulation -> increased HR, increased contractility, increased bp
HTN baroreceptor response Carotid massage
High BP -> increased stretch -> increased baroreceptor signal -> increased PNS stim -> decreased HR, decreased contractility, decreased bp
Arteriolar vasodilators
minoxidil and hydralazine
SE of hydralazine and minoxidil
Na and fluid retention
Arteriolar vasodilators cause hypotension -> decreased stretch -> increase SNS -> increase RAAS -> increased Na and water reabsorption
Maintenance dose formula
MD = (Cpss X Cl)/bioavailability fraction
Half life formula
t1/2= (0.7 X Vd) / Cl
Loading dose formula
LD = (Cpss X Vd)/ bioavailability fraction
Overweight woman OD on antiseizure meds w/ PMH of abortion of fetus w/ spina bifida. She is confused. What lab abnormaltiy would you expect?
Increased liver transaminases. Rare, but fatal hepatotoxicity (measure LFTs)
Would cause respiratory depression -> respiratory acidosis
Valproic acid SE
Teratogenic -NTD Hepatotoxicity Pancreatitis tremors wt gain
Mechanism of nitrates
NO activates guanylate cyclase -> increased cGMP-> activates myosin light chain phosphatase (MLCP) -> vascular smooth muscle relaxation
Also increased cGMP decreases intracellular Ca
NL Smoothe muscle contraction
Ca flows in and binds to myosin light chain kinase (MLCK) -> smooth muscle contraction
Phentolamine mechanism
Blocks alpha 1 -> vasodilation
Class 1 Na channel binding strength
1C>1A>1B
1B has the weakest Na binding. Dissociates quickly. Prefers ischemic tissue due to delayed switch from inactivated to resting state
Class 1C properties
Most use dependence
Has the greatest binding to Na channels
Slow dissociation allows the effects to accumulate -> arrhythmias
Opioid MOA - pre-synapse
Opiods bind to Mu receptors on presynaptic - block Ca channels -> decreased Ca-> decreased NT release
Opioid MOA post synapse
Bind to Mu receptors
Stimulate K efflux out of the cell -> hyperpolarization ( less likely to depolarize
Increased release of DA and NE from presynaptic nerve terminals. SE due to increased NE. Which sympathetic output will be affected: adrenal, eccrine sweat glands, bladder?
Sympathetic output to the bladder will be most affected.
Eccrine sweat glands and the adrenals get Ach released presynaptically to stimulate them. Other visceral organs get NE released presynaptically to stimulate them
Acute MI tx leads to wheezing. Which part of NT release is affected?
Epi is prevented from binding to B2-R to stimulate bronchodilation
B blockers block B2 -> bronchoconstriction -> asthma exacerbation
Nitroglycerin primarily affects which vessels
Large veins
Primary venodilator -> decreased preload
Constipation, bradycardia, AV block, and worsening heart failure after Afib txmnt
nondihydropyridine CCB (diltiazem and verapamil) SE AV block (chronotropic effect) worse Hf- negative inotropic effect
Dilitiazem and verapamil MOA
Block L-type Ca channels-> decrease phase 0. Slow Av conduction -> AV block
Canagliflozin MOA
blocks SGLT, which normally would reabsorb glucose
What should be checked before starting canagliflozin?
Check serum CR, should be avoided in pts w/ moderate or severe renal impairment
SE of SGLT inhibitors
UTI, increased sugar in the urine for bugs
Pt undergoes general anesthesia and has fever, jaundice, tender HM, centrilobular necrosis, and elevated LFT, and bili. What med caused this?
Desflurane, halothane, enflurane
Metabolized by CYP450 in the liver that creates active metabolites or immune-mediated hepatocellular damage
anti-u1RNP
MCTD -mixed connective tissue dz
Mixed connective tissue disease
Sx of SLE, systemic sclerosis, RA and polymyositis
Anti-La
anti SSB
Sjogren’s
anti ro
anti-SSA
Sjogrens
Pulsus alterans: What is it? What causes it?
Beat to beat variation in pulse amplitude
Commonly severe LV dysfxn
Dicrotic pulse: What is it? What causes it?
Pulse w/ 2 peaks, 1 for systole and 1 for diastole
Severe systolic dysfxn and high systemic arterial resistance
Hyperkinetic pulse: What is it? What causes it?
Rapidly rising pulse w/ high amplitude. Large SV against decreased afterload
Aortic regurg, AVM
Pulsus parvus et tardus What is it? What causes it?
Diminished SV (parvus) and prolonged LV ejection time (tardus) LVOT obstruction - Aortic stenosis
What causes angioedema in a woman who just started taking lisinopril?
ACEI leads to increased bradykinin, which increases vascular permeability
What should you suspect in a kid w/ angioedema?
C1 esterase inhibitor deficiency. Complement is hyperactive-> unregulated activation of kallikrein-> increased bradykinin
Kawasaki dz complication
coronary artery aneurysms
Rt arm and rt side of face swelling
Brachiocephalic vein obstruction
Face and arms swelling b/l
SVC syndrome
What defects can lead to a paradoxical embolus?
PFO, ASD, VSD
Why does a reperfusion injury lead to increased creatinine kinase
The cell membrane is damaged by reactive oxygen species and creatinin kinase is able to leak out of the cell
Murmur at the apex radiates to the axilla
Mitral regurg. The blood flows back to the pulmonary vessels
Murmur at the RSB radiates to the neck
Aorti stenosis- Increased flow of blood out to the carotids
Aorti regurg sound
Diastolic high pitched=twangy
“blowing” murmur. The blowing is subtle
What is transthyretin’s normal role?
Transport thyroxine and retinol
What can a mutation of TTR lead to?
Transthyretin can then misfold and become an amyloid that causes restrictive dz in the heart
3 day onset of progressive cough, orthopnea, dyspnea, and LE edema
Acute decompensated heart failure
CXR: Cephalization of pulmonary vessels, perihilar alveolar edema (batwing), costophrenic angle blunting, Kerley B lines
Acute decompensated heart failure w/ secondary pulmonary edema
Causes of ADHF
MI, severe HTN, valvular abnl, arrhtymias, cocaine
AV Fistula - Preload and afterload
Preload is increased - more blood coming back to the heart
Afterload is decreased - the fistula allows for some of the arterial pressure to be transferred to veins
What medication can increase peripheral vascular resistance, increase systolic bp, decrease pulse pressure, and decrease HR?
Phenylephrine (Alpha 1 agonist)
Vasoconstricts to increase peripheral resistance and systolic bp.
The HTN is sensed by baroreceptors, which activate PNS to decrease HR and SV -> decreased pulse pressure (smaller difference btwn systolic and diastolic)
What is decreased in the post-synaptic cells of pts w/ Myasthenia gravis?
The have Ab against Ach-R, so fewer ACh-R exist (removed due to complement) -> decreased motor end plat potential. A synapse still has the same potential, but the potential of the whole end-plate is reduced.
What would you use to improve diarrhea, nausea and abd cramping in a MG patient given pyridostigmine?
Scopolamine (anti-cholinergic)
Pilocarpine MOA
Muscarinic agonist
Hyoscamine MOA
Muscarinic antagonist like scopolamine
Carbonic monoxide findings: Carboxy Hgb, PaO2, methemoglobin
Carboxy Hgb increased
PaO2 NL
Methemoglobin NL
What can cause methemoglobinemia?
Dapsone (Dihydropteroate synthesis inhibitor-similar to sulfonamides. Use in leprosy), nitrites
RPF equation
RPF = RBF X (1-hematocrit)
Length constant of an AP?
Distance at which the originating potential decreases to 37% of its original amplitude
What does myelination do to the length constant?
Myelination lengthens the length constant so that a potential can get farther before it dissipates
Why would you hypoventilate a pt w/ cerebral edema?
Hypoventilation would decrease PaCO2, which is a potent vasodilatoer. Decreasing PaCO2 -> vasoconstriction and increased cerebral vascular resistance, Preventing further edema
Major causes of hypoxemia:
alveolar hypoventilation
NL A-a gradient, there is not enough O2 inspired in the air
Cause of hypoxemia:
V/Q mismatch
Increased A-a gradient. Obstruction in airway leads to decreased ventilation w/ NL perfusion
Cause of hypoxemia: Diffusion impairment
ie. alveolar hyaline membrane dz. Diffusion is prevented by a thickened alveolar capillary membrane
Cause of hypoxemia: right to left shunt
Deoxygenated blood from the right heart flows into systemic circulation -> decreased PaO2
In what cases is PaO2 decreased?
It is decreased in high altitude. There is less oxygen in the blood. Anemia, CO, and CN poisoning have nl PaO2
In what cases is SaO2 decreased?
CO poisoning and high altitude
CO competes with the O2 binding
High altitude there is just very little O2 to bind
Nl in anemia, CN poisoning, and polycythemia
In what cases is oxygen content (Hgb content and oxygen saturation) decreased?
High altitude - low O2 able to bind available Hgb
CO poisoning - Hgb is bound to CO, so very little O2 is bound to Hgb
Anemia - There is a low amount of Hgb, so even though O2 may be available there isn’t Hgb to bind to
Conductive hearing loss in right ear (describe PE)
BC>AC -abnl Rinne. The ear drum does not vibrate when the fork is put in the air, but does vibrate when put on the mastoid bone.
Localize to the right - Weber
The rt ear does not get ambient noise conduction and so it is better able to hear the resonation through bone
Sensorineural hearing loss on the right ear
AC> BC - NL Rinne Test. The nerve hears the sound just as poorly from the ear drum as direct contact
Localizes to the left -Weber
The rt ear has a damaged nerve, so it does not transmit the nerve impulse from bone conduction as well as the Nl ear
K percentages in Bowman’s, PCT, ascending loop, and collecting duct in NL person
Bowman’s -100%
PCT- 35%
Ascending- 10%
Collecting duct - 110%
What kind of receptors are Ca sensing receptors? What is a disorder of these receptors?
GPCR
Familial hypocalciuric hypercalcemia
Ca binds to CaSR and inhibits PTH Normally
Intrinsic Tyrosine kinase Receptors
Insulin
IGF- Insulin like growth factor
JAK STAT receptors
EPO
GH
cytokines
PRL
Marker of osteoblast activity
Bone specific alkaline phosphatase- synthesizing bone matrix leads to release of alkaline phosphatase
Markers of osteoclast activity
Tartrate resistant acid phosphatase
Urinary hydroxyproline
Urinary deoxypyridinoline
What does increased lung volume due to alveolar resistance?
Increased lung volume lengthens and narrows the alveoli - > increased alveolar vessel resistance
What does decreased lung volume due to extra-alveolar resistance?
Decreased lung volume
Extraalveolar lung vessels narrow due to chest cavity compression -> increased extra-alveolar resistance
Pulmonary vascular resistance equation
PVR= alveolar + extra-alveolar resistance
increased or decreased lung volumes increase PVR, lowest at FRC
RBF equation
RPF/ (1-hematocrit)
Deficient IL-12 would lead to a decrease in which cells and what cytokine could make up for it?
IL-12 activates Th1 cells. You could give IFN-gamma, which helps stimulate differentiation to Th1 and also is secreted by Th1
Nitroprusside’s effects on preload and afterload
Nitroprusside decreases preload and afterload through equal arteriole and vein dilation
Oval or round yeasts inside macrophages, Many small yeasts
Histoplasmosis is smallest btwn blasto and coccidiodes
Milrinone MOA
PDE-3 Inhibitor
Cardiac - Increased cAMP leads to increased cardiac muscle contraction
Vasculature - Increased cAMP leads to vasodilation
Which med would cause a greater increase in QRS complex at a higher HR?
Class 1C has the greatest use dependence. Will block Na channels more rapidly at higher HR and lengthen the QRS more at higher HR
22 yo ruptured cerebral anuerysm w/ extensive intracranial hemorrhage? Most likely congenital cardiac anomaly/
Adult type Aortic coarctation
increased risk of berry aneursyms and aortic HTN
Hyperlipidemia drug causes flushing, what mediates the SE?
Niacin causes flushing via PGD2 and PGE2. Give aspirin (Cox inhibitor) before niacin to decrease flushing
How to prevent Group B strep in an infant?
There is no vaccine for GBS. You give the mom ampicillin to clear the infxn during pregnancy
Bosentan MOA
Endothelin receptor antagonist. Blocks vasoconstricting effects of endothelin
Bosentan used for?
Idiopathic Pulmonary artery HTN
What pt dz would cause anaphylaxis when giving O negative RBCs?
IgA deficiency
Develop IgE against IgA (anti-IgA). The RBCS may have a small amount of IgG that triggers anaphylaxis
Chronic rejection of a lung allograft damages where?
Small airways, Bronchiolitis obliterans. Solid organs-vascular obliteration
Which segment in the lungs has the greatest airway resistance?
The medium sized bronchioles - due to highly turbulent flow
Which segment has the lowest airway resistance?
Terminal bronchioles - increased cross-sectional area
Cough reflex afferent and efferent
Afferent is internal laryngeal n. (sensory-branch of CN 10) in piriform recess
Efferent is CN 10
Hyperoxia in COPD pt leads to what effect on V/Q?
Hyperoxia leads to vasodilation, which creates alveoli that are now ventilated with poor perfusion. Increased physiologic dead space
Hypoxia affect in COPD on vasculature
Hypoxia causes vasoconstriction of vessels supplying alveoli w/ low O2 content, perfusion is saved for the alveoli that are well ventillated
Whats causes a brown pigment stone?
Biliary tract infxn
Injured hepatocytes and bacteria release beta-glucuronidase, which breaks down bilirubin glucuronide ->increased Unconjugated bili
What causes black pigment stones?
Chronic hemolysis (SCA or spherocytosis) Ileal dz - increased enterohepatic cycling of bili
Inhibition of 7 alpha hydroxylase, what drug and MOA?
Fibrates inhibit 7-alpha-hydroxylase
Reduce conversion of cholesterol to bile acids -> lower solubility of cholesterol stones
What kind of liver dz has decreased serum albumin?
Chronic end stage liver dz
The remaining hepatocytes have reduced fxn, albumin has long half life (20 days)
What kind of liver dz causes distended abdominal veins, ascites, and palmar erythema?
End stage liver dz (cirrhosis), due to portal HTN and increased estrogen
What kind of liver dz causes splenomegaly?
Portal HTN causes blood to flow to Splenic vein since portal vein is blocked
What kind of liver dz causes a prolonged PT time, elevated aminotransferases, leukocytosis, and eosinophilia, and NL albumin?
Acute fulminant hepatitis
Halothane hepatotoxicity is indistinguishable from acute fulminant viral hepatitis on histology
Pt has any kind of surgery somewhere besides USA and develops and dies from liver issues. What pattern of injury?
Hepatocellular pattern
Rapid liver atrophy (shrunken)
Hepatocellular pattern of injury on histo
Widespread centrilobular necrosis
Inflammation of the portal tracts and parenchyma
Mechanism of halogenated anesthetic heptotoxicity
Hypersensitivity to the drug causes immune mediated attack against hepatocytes
Nerves innervating EAC
Posterior is auricular branch of vagus, and the rest is auriculotemporal of mandibular (V3)
Medical Tx of biliary colic
Ursodeoxycholic acid (hydrophilic bile acids) increase bile solubility and reduce cholesterol secretion
Cholestyramine and risk of gallstones
No net risk
Decrease enterohepatic recirculation of bile acids (less soluble cholesterol increased risk)
Stim conversion of cholesterol to bile acid and increase gallbladder motility (decreased risk)
Fibrate MOA
Upregulate LPL -> clear LDL
Activate PPAR-gamma to increase HDL synthesis
Inhibit 7-alpha-hydroxylase -> decreased conversion of cholesterol to bile acid (increased cholesterol stone risk)
Diphenoxylate MOA
Mu opioid -decrease GI motility
What drugs is diphenoxylate combine with? Why?
It is combined w/ atropine to cause dry mouth, blurry vision, and nausea (anticholinergic) at high doses to discourage excessive use
Meperidine MOA
Mu opioid- decrease GI motility
Loperamide MOA
Low dose Mu opioid agonist
Hepatic abscess via hematogenous seeding, what bug
Staph Aureus
Total gastrectomy requires lifelong administration of?
Vitamin B12 (water soluble) Lack of IF to bind B12 and facilitate absorption
Kid gets recurring giardiasis what enzyme will be deficient due to inflammation and infxn?
Secondary lactase deficiency
Also possible w/ celiac dz
Theophylline MOA and toxicity
PDEI - similar to cortical stimulant effects of caffeine, used for bronchodilation
Can cause sz and tachyarrhythmia due to caffeine like effects
Months of fatigue, rash (worse after hot showers), flushing, abd cramps, dizziness, syncope, and mast cells positive for KIT
Systemic mastoytosis
Increased mast cells w/ KIT (tyrosine kinase) mutation. Excessive tryptase and histamine
What does excess histamine cause in systemic mastocytosis?
Syncope, flushing, hypotension, pruritus, urticaria, and increased gastric acid secretion
What is the mechanism behind Zenker’s diverticulum?
Cricopharyngeal motor dysfxn
Cricopharyngeus doesn’t relax leading to increased oropharyngeal intraluminal pressure-> herniation-> false diverticulum
Anti-mitochondrial Ab
Primary biliary cholangitis
Lymphocytic infiltration and destruction of small intrahepatic bile ducts (2 possible causes)
Primary biliary cirrhosis
Graft versus host dz
Acetaminophen OD histo
Centrilobular necrosis that can extend to include the entire lobe
Acetaminophen OD tx
N-acetyl-cysteine, regenerates the decreased glutathione
Acetaminophen common drug name and where it acts
Tylenol, mostly in the CNS Cox3, less GI SE
Acetaminophen OD pathology
Acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic byproducts in the liver
Hepatocellular swelling and necrosis, Mallory bodies, neutrophilic infiltration, and fibrosis. What caused this?
Alcoholoic hepatitis
What is a mallory body?
Cytoplasmic inclusion in heptocytes made up of damaged intermediate filament
Hepatomegaly w/ tense capsule and reddish-purple parenchyma, severe centrilobular congestion and necrosis
Budd-Chiari Syndrome
Hepatic vein obstruction
Non-inflammatory hepatocyte necrosis w/ fibrosis
Hemochromatosis
Liver histo - Panlobular microvesicular steatosis
Reye Syndrome
What is reye syndrome?
Give aspirin to a kid w/ a viral infxn
encephalopathy and liver dz
Reye syndrome mechanism
Aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzymes
Reye Syndrome findings
Mitochondrial abnormalities, microvesicular fatty liver, hypoglycemia, vomiting, hepatomegaly, coma
What viruses is Reye syndrome associated with?
VZV and Influenza B
Pernicious anemia effect on gastrin, gastric pH, and parietal cell mass
Parietal cell mass low -> decreased gastric acid (high gastric pH) and decreased IF (B12 deficiency)
Leads to increased gastrin secretion from gastric G cells
What part of HDV life cycle is supported by previous HBV?
HBV provides the coating of HDV particles allowing it to penetrate a hepatocyte
Name products of TCA cycle
Pyruvate -> acetyl CoA-> citrate->isocitrate->alpha-ketoglutarate->succinyl Coa->succinate-> fumarate->malate-> oxaloacetate
Pyruvate kinase
PEP to pyruvate
Pyruvate dehydrogenase and what cofactors are required
Pyruvate to acetyl CoA
requires thiamine (decarboxylase)
B2-riboflavin, B3- niacin, B5-pantothenic acid, lipoic acid
Citrate Synthase
Oxaloacetate + acetyl CoA to citrate
Aconitase
Citrate to isocitrate
Isocitrate dehydrogenase
What Cofactor
Isocitrate to alpha-ketoglutarate
requires niacin as NAD+ -> NADH
Alpha-ketoglutarate dehydrogenase. What cofactors?
Alpha-ketoglutarate to succinyl CoA
Requires Thiamine(B1)
B2-riboflavin, B3-niacin (NAD+-> NADH), B5-patothenic acid, and lipoic aicd
Succinate thiokinase
Cofactor
AKA Succinyl-CoA synthetase
Succinyl-CoA to succinate
Requires GDP-> GTP
Succinate dehydrogenase
What Cofactor
Succinate to fumarate
Requires B2-riboflavin
FAD+->FADH
Fumarase
Fumarate to malate
Malate dehydrogenase
Cofactor?
Malate to oxaloacetate Requires niacin (NAD+-> NADH)
Pyruvate carboxylase
Cofactor?
Pyruvate to oxaloacetate for gluconeogenesis Requires Biotin (carboxylase)
What are the defense mechanisms against giardiasis?
IgA prevents adherence
and CD4 Th Cells
2 Major causes of polyhydramnios
Impaired fetal swallowing or increased fetal urination
2 main Causes of decreased fetal swallowing leading to polyhydramnios
GI obstruction - esophageal, duodenal, or intestinal atresia
Anencephaly - No brain to coordinate swallowing
Pregnant pt w/ epilepsy what is the baby at risk for
Valproate, carbamazepine, phenytoin -> increase risk of NTD
Pulmonary hyoplasia is cause or result of what?
It is a result of oligohydramnios, possibly due to renal agenesis. Low volume of urine made leads to low amount of amniotic fluid-> poor lung development
Ipratropium MOA
Anti-muscarinic - bronchodilation
Magnesium sulfate in asthma MOA
Inhibits Ca influx -> bronchodilation
Stabilizes T cells
Inhibits mast cell degranulation
What does pulmonary edema due to compliance and surface tension, and FRC?
Fluid in the alveoli increases air resistance -> decreased compliance
Surface tension increases w/ fluid in the alveoli->decreased compliance-> alveoli more likely to collapse -atelectasis
The decreased compliance means the lungs can’t fill as well-> decreased FRC and decreased TLC
Atrialization of the right ventricle (Epstein’s anomaly) is associated with what med?
Lithium used for bipolar
General classes used to treat bipolar disorder, schizophrenia, and epilepsy
Bipolar - lithium and mood stabilizers like valproic acid, carbamazepine, and atypical antipsychotics
Schizophrenia - antipsychotics (haloperidol, fluphenazine) atypicals (aripiprizole, clozapine)
Epilepsy (valproate, phenytoin, carbamazepine)
Bipolar tx
Lithium
Carbamazepine
Valproate
Atypical antipsychotics(aripiprazole and zapines)
Schizophrenia Tx
Haloperidol, fluphenazine
atypical - apiprazole, clozapine
Epilepsy Tx
Valproate, carbamazepine, phenytoin
Child has vascular lesions w/ IgA and C3 deposition
Henloch Schonlein Purpura -
Purpuric rash (butt)
colicky abd pn, polyarthralgia
Vasculitis: Saddle nose and olguria
Granulamatosis with polyangitis
Vasculitis: Weak upper extremity pulses
Takayasu arteritis - aorta and its branches
Vasculitis: HA and blurred vision
GCA
What cells release histamine and tryptase?
Histamine- basophils and mast cells
Tryptase - Mast cells only
Multiple cystic edematous hydropic villi, P57 negative
Complete mole,p57 negative=absence of maternal genome, all dad
Carcinoembryonic antigen
colorectal maliignancy
CA-125
Ovarian CA
Sarcoma botryoides in a young girl
Bunch of grapes out of vagina
rhabdomyosarcoma arising from the bladdeer or vaginal mucosa
CA 19-9
Pancreatic CA
C3b fxn
Opsonin and activates MAC
5-HETE (5-hydroxyicosatetraenoic acid) fxn
LT and lipoxin precursor
Neutrophil and Macrophage chemotaxis
Neutrophil degranulation
C5A fxn
Chemotaxis and increased phagocytosis directly
LTB4
Chemotaxis
Opsonins
IgG, C3B, CRP, and mannose binding lectin
Which hormones have the same alpha subunit?
Hcg, TSH, FSH, LH
Which hormones have beta subunits with significant homology?
Hcg and TSH
Painless scrotal mass, increased sweating and heat intolerance, increased T4 and T3, hypoechoic mass w/in the testicle
Testicular germ cell tumor secreting Hcg which can bind TSH -R if excessive enough
How do cancers met to the skeletal system?
Hematogeneous spread not lymphatic
Prostatic venous plexus receives blood from where?
Prostate, penis, bladder
Preventable adverse event
Harm to pt due to failure to follow EBM
Near miss
No harm to pt, prevented before harm could take place
Atypical endometrial cells, disorganized glands, and multiple mitoses
Endometrial adenocarcinoma commonly in post-menopausal women
Dilated, coiled endometrial glands and edematous stroma
Common during the luteal phase
Pathologic- ectopic pregnancy will stimulate this luteal phase due to the corpus luteum, but no implantation in the uterus