High Yield Flashcards
In hypovolemic shock, you give fluids to do what two things:
- Increase preload (extend end diastolic sarcomere length of the myocardium).
- Decrease sympathetic response of TPR
Coronary autoregulation via two things:
- NO* (released in response to NE, AcH, endothelinin, bradykinin, histamine)
- adenosine
Cardiac Catheterization:
Pulmonary Cathet. Wedge Pressure = Left atrium end diastolic pressure = pulmonary artery pressure distal to site of occlusion
Normal: LAEDP = LVEDP
Mitral stenosis: High LAEDP / Pulm Wedge > LVDEP
Aortic Stenosis: High LVDEP
Paroxysmal supraventricular tachycardia
- most common paroxysmal
- Similar to A -fib: Due to re-entrant impulses traveling through both slow and fast segments of AV node.
Dx: Sudden HTN, Tachy, palpations
Tx: Carotid massage: increase parasymph NS –> prolongs AV node –> slows HR. (risk syncope!)
If not a choice, think:
- Pheochromocytoma (with periodic H/A)
- Cocaine (with dilated pupils and chest pain = NE inhibited repute ant post synaptic cleft)
bobbing head + diastolic high pitch murmur
Aortic regurgitation: back flow (hence diastolic)
Marfans, SLE, RHA, endocarditis, syphillus, ankylosing spondylitis
diastolic rumbling murmur over heart apex + opening snap
Mitral valve stenosis: valve opening
Explain Thyroid hormone synthesis
- Thyroid follicles oxidize Iodide –> Iodine in the lumen
- In the Thyroglobulin via thyroid peroxidase: Iodine + tyrosine –> MIT + DIT (di-iodo-tyrosine)
DIT + DIT –> T4
DIT + MIT –> T3 - Thyroglobulin now has I2 + T4 + T3 + MIT + DIT and is ingested as a whole by lysosomes
- Iodotyrosine deiodinase recycles iodine from left over MIT and DIT AND causes T4 –> T3 –> rT3 (inactive) , for more T3 (peripheral tissue)
thyroid hormone axis
Hypothalamus (teritiary)–> TRH –> Anterior Pit. (secondary) –> TSH –> Thyroid gland (primary hypothyroidism = Hashimoto) –> T3/T4
Tan Adipose
- Fetal Adipose
- [Mt] = hogh O2 requirements = high capillaries
- Heat (No ATP) production via thermogen in oxidative phosphor. of UNCOUPLED ETC.
Gestation week with highest hCG
Week 9 (trophoblast) - maintains corpus lute until placenta develops (estrogen)
Human Placental Lactogen (hPL)
- trophoblast
- causes insulin resistance + lipolysis –> high glucose + FA + ketones to be sent to fetus
- Risk gestational diabetes when pancreas can’t overcome hPL.
Anovulation
- when the hypothal-pit-ovarian axis isn’t working
- ovarian follicle is released and turns into the corpus lute, but doesn’t make progesterone (although High Estrogen due to active ovaries)
- Endometrium remains in proliferative stage = irregular menstruation
Confirm menopause
-no estrogen = no active ovaries = no feed back = high FSH (early) + LH (later)
Neurophysins
Carry signals from hypothalamus to posterior pituitary gland: ADH (supraoptic nuclei) + Oxytocin (paraventricular nuclei)
Secretin
- Released from pancreas and stomach
- Peptide hormone for water hemostasis
- Acidic –> S cells –> secretin –> Duodenum–> basic
Pancreatic Juices
- Secretin
- HCO3
- Normal Na and K
- Low Cl
Trypsin (Trypsinogen) –> activates chemotrypisin, phospholipase A2 and eleastase
Lipase: Lipids –> FA
Amylase: poly (starch) –> monosaccharides (2 glucose)
Stomach acid secretion 3 stages
- Cephalic = smell/though = cholinergic + vagal
- Gastric = Gastrin = Histamine
- Intestinal = protein in duodenum = peptide YY causes low acid secretion
40 + fat + female
Post fatty meal = Cholysitis
- Gall stones (i.e. biliary colic).
Risk: necrotic gallbladder = acute calculous cholecystitis (gallbladder obstruction at the cystic duct –> ischemic mucosal layer disruption –> bacterial invasion)
Mechanisms:
A) when fat enters duodenum (site of lipid resorption), I cells in duodenum and jejunum make Cholecystokinin which causes gallbladder contraction and stasis –> bile concentration –> sludge –> cholesterol stones
B) High Estrogen and Progesterone:
E –> cholesterol synthesis –> liver HMG-Coa reductase –> bile + insoluble cholesterol –> bile salts + phosphotidycholine + small water soluble cholesterol (via 7-alpha-hydroxylase)
P –> slows bile secretion –> slows gallbladder emptying
C) when 7-alpha-hydroxylase is impaired, cholesterol cannot become water soluble
D) Chrons Disease = terminal ileum inflammation –> transmural inflammation (NF-KB = cytokines = inflamm) –>
(1) stricture --> no site of bile acids recycling for FA digestion = thus bile salt has a higher ratio of cholesterol to bile acid = cholesterol ppt due to bile acid wasting (2) fistulas --> caused from inflammation which lead to ulcers. (3) non-caseating granulomas (like sarcoidosis)
In ulcerative colitis, its not transmural (only mucosa and submucosa) inflammation. Thus no fistulas forms. Has continuous mucosal damage with the rectum always involved. Bloody Diarrhea with or without ab pain. Churns Disease always has ab pain.
E) Gallstone at ileocecal valve = gallstone ileus = air in biliary tree (not calcified pancreas which is chronic pancreatitis)
F) Black pigmented gallstones = unconjugated bilirubin precipitates as calcium bilirubinate due to chronic hemolysis
Morphine mechanism
- mu receptor –> 2nd messenger C coupled –> K efflux and low Ca influx –> hyper polarization at post synaptic.
- tolerance is via glutamate
Hep A person with IgM means what?
Re-infection
Jugular vein distention + low BP + High HR
Cardia Tamponade
Bicuspid aortic valve causes
- Sudden infant death
2. the usually tricuspid arctic valves will eventually use aortic stenosis in the 50’s
Kidney Stone composition
normal blood Ca + High urine Ca
(High blood Ca + Urine Ca = HyperPTH or sarcoidosis)
High oxalalate intestinal resorption
- Renal canaliculi causes stones
- You need P, Ca, low water, acid,
- High citrate will prevent it
COLA amino acids (Cysteine, ornithine, lysine, arginine) will result in stones
Cysteinuria = hexagonal shaped crystals in urine = Amino Aciduria
- COLA amino acids can’t be reabsorbed in the proximal renal tubes, leading to supersaturation and hence cystine stones
NOTE: Other kidney stone causes:
- Hypercalciuria (Sarcoidosis)
- Hyperoxaluria (Chron’s)
- Hyperuricosuria (Gout)
- Hypocitraturia (Distal tubular acidosis)
- Hyperaciduria (Cystien)
Pyelonephritis
Urine back flow (vesicouretal junction) into the kidneys
- Leads to UTI in women
Labs show high WBC counts
Myasthemia Gravis
- Antibodies destroy AcH receptors at post synaptic cleft (overall synaptic AcH remains the same) –> no motor end plate potential –> no muscle depolarization
- Muscle weakness (Eye movement gets worse with activity, but rest relieves symptoms)
Tx: Anti-cholinesterase (increase AcH), If causes GI issues you must use a muscarinic receptor antagonist = scopolamine.
provoke asthma
Methacholine, histamine or cold air
Alpha-q-antitrypsin deficiency
emphysema or COPD (low elastase/anti-protease)
Lung infection (cough/sputum) + dyspnea
COPD or emphysema
- Air is obstructed due to no elastin in bronchus and low alveolus (low surface area)
Chest X-ray shows flat diaphragm or hyper inflated lungs
COPD or emphysema
- inflated lungs are due gas being stuck due to air flow resistance
4 causes of hypoxia
- Hypoventilation (Resp. Acidosis)
- Ventilation-Profusion mismatch (V/Q): embolism (Resp. alkalosis)
- R to L shunt
- Diffusion impairment: pulmonary fibrosis, end stage lung cancer, emphysema, exercise
Spirometry shows what in COPD patients
- Low FEV1/FVC ratio
Restrictive lung diseases such as pulmonary fibrosis will show a
LOW FRC (functional residual capacity = RV + ERV)
Interstitial lung disease will be at risk for:
pulmonary fibrosis
Bronchitis + dyspnea + diffuse lung radiopacities
Interstitial fibrosis
- Has elastic recoiling (wide air way = radial traction, or outward pulling by fibrotic tissue, on airway walls)
Opposite of COPD Dx:
- High FEV1/FVC
- Low FRC, TLC, RV
High RR + Low Tidal Volume
Pulmonary fibrosis
High Lung compliance =
Low Lung complaince =
A. Emphysema (low elastic)
B. Pulmonary fibrosis (High elastic)
Paget Disease
Defect in bone metabolism: Osteoclast –> mixed phase –> osteoblast = bone over growth / mosaic lamellar bone that is dense but hypo vascular = weaker = prone to fracture
- High alkaline phosphatase (osteoblast)
- bone pain
Risk: Osteosarcoma
ADH acts via two mechanisms
V1 –> vasoconstriction of blood vessels -> increase BP
V2 –> medulla collecting duct –> cAMP –> aquaporin 2 –> ADH response (high urea, low water) –> decrease osmolality –> increase BP
Calculate renal blood flow
- Use PAH (proximal duct secretion OR K+ collecting duct resulting in amount excreted > amount filtered)
- RBF = RPF / 1 - hematocrit)
where RPF = PAH clearance = (urine [PAH] x urine flow / plasma [PAH])
mast cells will cause what in the bowel?
mast cell –> histamine (H2 receptors and increase cAMP) –> Gastric hyper secretion.
Other gastric acid stimulators:
1. AcH or grastrin + M3 receptor –> Ca+
High Ca + cancer
PTH related peptide (not PTH alone) = humoral hypercalcemia of malignancy
Normal Ca and PTH levels, but fracture prone
osteoporosis
multinucleus cells from bone
osteoclasts
- Think paget disease if presented with multiple areas of bone pain
Frothy urine
proteinuria or bile salts in urine
ACE inhibitor mechanism
- Elanopril
- Decrease Angio II
Remember Angio II causes:
- vasoconstriction of EFFERENT a.
- increase adrenal cortical aldosterone
Abdominal pain + red urine after standing for 24 hours + normal liver
Porphyrin synthesis abnormality
Tx: Dextrose
Urinary incontinence causes
- Surge (laugh) = high ab. pressure > sphinctor OR urethral issue
- Urge (frequency) = over-activation detrusor
- Overflow (dripping or unfinished urination) = low detrusor contraction OR bladder obstruction (tumor > 50 yrs)
high 5-HIAA in urine
metastatic carcinoma
Deficient CD55, CD59
Paroxysmal nocturnal hemoglbinuria
- Causes complement activation
RBC without central pallor
spherocytosis
- mild dehydration of the RBC
- RBC membrane cytoskeleton abnormalities (spectrin, ankyrin)
- causes high MCV
RISK: parovirus B19 infection, spleenomegaly, anemia, jaundice
high lactate dehydrogenase
Hemolysis
Ex: hemolytic anemia
Also seen in idiopathic membranous nephropathy due to renal vein thrombosis (due to loss of antithrombin III that is lost, along with other things, with the high capillary permeability found in nephrotic syndromes )
High gamma globulin
M protein with high monoclonal immunoglobulins
Ex: multiple myeloma (plasma cell neoplasm)
Microcytic vs macrocytic anemia
Micro = Fe deficiency Macro = VB12 or folate deficiency = hyper-segmented PMN. Its VB12 when you have neurological symptoms (i.e. decreases sensation)
Hypotension, Tachy, Rapid Breath, High/Low temp (fever)
OR
fever + chills + high BC + High PMN
Septic Shock (TNF-alpha) - in sickle cell patients--> splenic --> encapsulated bacteria will cause septic shock = Step. pneumonia or Hem. influenza
vascular lesion + IgA + C3
OR
child + develops after a respiratory disease + bloody stools + bloody urine + palpable skin lesions
Type of immune complex vasculitis called Henoch-Schonlein purpora (most common small vessel vasculitis in children)
- Systemic hypersensitivity rxn
- Presents with rash (palpable purpura), ab pain (GI pain), polyarthralgia (joint pain)
- Risk: Glomerulonephritis
White pupillary reflex
Retinoblastoma (most common childhood eye cancer)
Mutations of two Rb genes
Risk: Osteosarcoma
Ewing Sarcoma
long and flat bones of children
- neuroectoderm
- May resemble acute osteomyelitis
medullablastoma
most common childhood malignant brain tumor of the cerebellum
immobile sperm
Primary Ciliary Diskinesia
- Form of Kartagner Syndrome
- Impaired dyne arms
- Clinical: infertility + bronchial dilation + sinusitis
Ventircular hypertrophy is seen in
- HTN
- Hemolytic anemia (due to Fe deposits)
- Cardiomyopathy
- CHF
- Ischemic heart disease (results in heart failure)
Note: normal aging decreases heart size, causing sigmoid shape septums
Vaginal discharge + positive pregnancy test + normal villi + triploid karyotype
partial mole (low risk cancer)
NOTE: complete mole (high risk cancer)
Vaginal discharge + no positive pregnancy + 46XX or XY + trophoblast grape clusters
Both have trophoblast
S3 + holosystolic over heart apex + dyspnea + lung crackers + meds solve symptoms
functional mitral regurgitation (Tx: Diuretics which decrease EDV of the Left ventricle)
- When meds do not solve issue –> chorda tindinae rupture issue with infective endocarditis
Artheroscelrotic plaque MI risk
the plaque has a fibrous cap that is constantly being remodeled by macrophages, which degrade the college via mettaloproteinases (NOTE: the body responds by dilating the arteries…the body has time to do so because the plaque is slowly growing)
Lysyl oxidase strengthens the collagen cap!
Plaque over-all mechanism:
endothelial injury –> endothelial permeability –> leukocyte attachment + platelet + growth factors + cytokines –> smooth cells migrate from intima media
Tx: adenosine or dipurimadole
- increase in arteriole dilation. This causes more flow to normal tissue, and less to the already maximally dilated artieries affecting ischemic tissue
Body protects against platelet aggregation via endothelium secretion of prostacyclin
Irreversible Injury = Mt with vacuoles or phospholipids –> can’t produce ATP via oxid. phosph
Zollinger-Ellison syndrome
PUD –> Gastrinoma risk (Gastric acid tumors of the pancreas)
- G cells = gastrin = gastric acid
Dx: High gastrin levels in response to secretin release (Should be opposite)
NOTE: VI peptide (Vasoactive Intestinal) is made by pancreas islet and gastric mucosa to relax GI smooth muscle, inhibit acid, and stimulate bicarb from pancreas (like secretin).
Duodenum S cells = Secretin = FA activity in duodenum = causes pancreas and bile to release bicarb = decrease acidity
Somatostatin Delta cells = decrease acid and all GI hormones
Other causes of Ulcers in duodenum = H. pylori, NSAIDs (But should see high gastric acid with low secretin)
PUD Hx + high alkaline phosphatase (bile tree destruction) + onion skin histology = sclerosing cholangitis
somatostatin
decreases all GI hormone (gastrin, secretin, VI peptide, cholecsyokinin)
Without somatostatin (Delta Cells) –> High gastrin –> parietal cells release acid –> duodenal ulcers
Types of diarrhea
- secretory = tea colored + odorless (VIPomas)
- inflammatory = pus + blood
- osmotic = lactose/diet intolerance
Tea colored diarrhea + odorless
VIPomas
High bilirubin + death
think Crippler-Najjar syndrome
- No UGT (uridinediphosphate-glucornyl-transferase) enzyme from conduction in liver ER.
HIV + blurred vision
CMV induced retinitis from retinal detachment due to tearing of thin, scar tissue post inflammation
Tx: Ganciclovir (similar to acyclovir but is stronger specifically against CMV DNA polymerase)
older person + progressive vision loss + gray macula
age related macular degeneration
Types:
- Wet = Acute vision loss within weeks (ECM accumulation –> hypoxia –> vascular endothelial growth factor + gray/green retina
- Dry = gradual vision loss (oxidative retina pigment damage) + retinal duress deposits
painful swallowing
esophagitis (in HIV, think CMV, candida or HSV-1)
pneumonocystic pneumonia
Pneumonocystis jiroveci (only occurs in immunocompromised patients)
periodic + long duration + large amplitude + non-peristalic
Angina Pectoris
inability of the lower esophageal sphincter to relax during swallowing
Achalasia
- relaxing of the LES is to allow the food bolus travel to the stomach.
- In achalasia, the LES is elevated to prevent this.
NOTE:
- cricopharyngeal m. is in the UES which contracts to push the food bolus into the esophagus resulting in inability to swallow = choking sensation
- uncoordinated contractions results in diffuse esophageal spasms with non-cardiac chest pains
- GERD: opposite of achalasia
Alcoholic that persistently vomits + mucosal wall tears
Mallord-Weiss tears
- upper esophagogastric junction mucosal tear
- leads to metabolic alkalosis (loss of gastric acid)
High serum iron + hereditary
Hemochromatosis
- Intestinal absorption
excess copper is excreted via
hepatic excretion into bile
- Accumulation of copper in the organs (i.e. brain and eyes = Kayer-Fleischer rings of copper in cornea) is Wilson’s Disease. Also see low ceruloplasmin, test via slit lamp exam.
Bright red blood in vomit
GI bleed –> Nitrogen –> converts to ammonia for urea release
Liver Cirrhosis
Gynecomastia (liver can’t metabolize estrogen)
Edema
Ascites
Spider angiomata (high estradiol)
testicular atrophy / low body hair (high estradiol)
hepatic encephalopathy
malodorous breath (no ammonia recycling)
Portal HTN = esophageal varices, spleenmegaly
ischemic effect of myocardial cells at 60 sec and 30 min
60 sec = loss of contractility
30 min = irreversible damage due to loss of 50% [adenine]
serum creatinine kinase
cell membrane damage in heart, brain, skeletal muscle (i.e. from ischemia, DVT)
CHF + drug dilates arterioles and veins + diuretic
Natriuretic peptide
Types:
ANP = Aorta
BNP = Ventricles
Released in response to volume overload (i.e. CHF) to act as vasodilation –> ventricular hypertrophy
Dyspnea + must sleep upright
CHF
Mechanism: low renal BP –> low GFR of macula dense –> renin is secreted –> liver secretes angiotensinogen –> Angio I –> ACE converts Angio I to Angio II –> vasoconstriction (increase arteriolar resistance) + aldosterone + sodium retnetion (water retained)
Uterus “bunches of grapes”
Hydatidiform mole
- from trophoblast obliteration
Dx: vaginal bleeding + nausea
Risk: Choriocarconoma (monitor B-HcG)
Pre-ecamlampsia + seizures
Eclampsia
Pregnancy + HTN + edema (leg swelling) + Protenuria
Pre-Eclampsia
- RISK: HEELP
Hemolytic Anemia
Elelvated liver enzymes
Low Platelets
Endometrial hyperplasia
Think high Estrogen levels (supplements or tumor = granolas cell tumor)
female with facial hair and acne
High androgen levels
obesity + facial hair + abnormal menstruation
Polycycstic Ovarian Syndrome
- Obesity = insulin resistance
- Facial hair = androgens
RISK: DM II and endometrial adenocarcinoma
Adnexal Mass
CA-125 = Malignant ovarian epithelial tumor
due to high number of ovulations. Thus, lower number of ovulation (with oral contraceptives) result in lower cancer risk
Remember, CA-125 is a poor marker for only ovarian cancer since it codes for cervix, endometrium, fallopian tube cancers)
High CEA
colorectal and pancreatic tumor
High B-HcG
Pregnancy, trophoblast tumors (Hyadtidiform, choriocarcinomas)
High DHEA
Adrenal tumor
Cervical Intraepithelial Neoplasia III (CIN III)
HPV 16, 18 (Sex)
Female with Hx of PID + ammenhorea + vaginal bleeding
Ectopic Pregnancy = vaginal enlarged (but Uterus is NOT enlarged), soft uterus = hormones mimic normal pregnancy = decidualized endometrium WITHOUT embryonic tissue or chorion
normal appearing endometrial glands + enlarged uterus
Adenomyosis (Not ectopic pregnancy bc pt does not have enlarged uterus)
post menopause + abnormal bleeding
think Adenocarcinoma
- Menopause = 50 years old
Hypotension + Tachy + Fever / low temp + low Na + high K + hypoglycemia
Shock + low Na + high K + low glucose = Adrenal Crisis (ie. Adrenal Hemorrhage)
child + fever + vomit + nuchal rigidity + rash
meningococcal meningitis (N. gonohrrea)
meningococcal meningitis + adrenal crisis
Waterhouse-Friderichsen syndrome
Meningitis = Child + vomit + nuchal rigidity + rash
Adrenal Crisis: Hypotension + tacky + fever + low Na + high K + low glucose
brain base
sella turcica = anterior (Rathkes pouch) and posterior (hypothalamus neurons) pituitary
RISK: craniopharyngiomas of the Rathke’s Pouch
most common thyroid cancer
papillary carcinoma
Long fingers + arms exceeding height
Marfanoid Syndrome (Also could be MEN2 if with mucosal neuromas which are flesh colored nodules on lips and tongue; along with thyroid mass)
Risk:Medial degeneration –> Aortic disease (Aortic regurgitation/aneurysm)
Thyroid nodule + High Calcitonin
Medullary Thyroid Cancer (Parafollicular C cells)
High 17-hydroxyprogesterone + testosterone + very early puberty
21-hydroxylase deficiency (adrenal cortical hyperplasia)
- NOT Leydig cell tumors
High catecholamines
Adrenal medullary hyperplasia
High TSH + Low T3/T4 + enlarged thyroid gland
Hypothyroidism (Hashimoto’s = mononuclear infiltrate into well defined germinal centers = lack of iodine)
lower leg skin thickening and induration
Hyperthyroidism (Grave’s Disease)
most common anterior pituitary gland tumor
Lactotroph (prolactin)
MEN1 tumors
3 Ps = Pituitary, Parathyroid, Pancrease
Highest risk for DM patients
Coronary artery disease (MI)