First Aid Pics II Flashcards
What is SMA syndrome?
SMA syndrome = transverse (distal 1/3) portion of the duodenum is entrapped btwn the SMA and the aorta causing intestinal obstruction
Location of Meissner vs. Auerbach plexus
Meissner = submucosal nerve plexus- located in the submucosa (first layer right under the mucosa)
Auerbach = in the muscularis propria
Specific change seen in Barrett’s esophagus
Barrett’s esophagus = a type of metaplasia = change in stress on a cell type changes the type of cell
Stem cells change from making nonkeratinized stratified squamous cells to making intestinal epithelium (nonciliated columnar ep. w/ goblet cells) that is more adapted to deal w/ gastric acid
What is this CT w/ oral contrast showing?
Narrowing of the distal duodenum- 2/2 circumferential ectopic pancreatic tissue = annular pancreas
Differentiate the venous drainage above vs. below the pectinate line
Above pectinate line: enters IVC thru inferior mesenteric vein from the superior rectal vein
Below pectinate line: enters IVC thru the common iliac vein from the inferior rectal vein
Using ‘SAD PUCKER’ mneumonic, name the GI retroperitoneal structures
Suprarenal (adrenal) gland
Aorta and IVC
Duodenum (parts 2,3,4)
Pancreas (except the tail)
Ureter
Colon (descending and ascending)
Kidneys
Esophagus
Rectum
Which type of hernia is in each of the 3 X’ed areas
- Lateral to inferior epigastric vessels = indirect inguinal hernia
- Medial to inferior epigastric vessels (in Hasselbach’s triangle) = direct inguinal hernia
- Inferior to inguinal ligament = Femoral hernia
Explain how a gallstone can cause both cholangitis and pancreatitis
If gallstone sits at the ampulla of Vater it blocks both the common bile duct and the pancreatic duct (double duct sign)
What happens to bilirubin after conjugation in the liver?
Gut bacteria converts it into urobilinogen
80% of urobilinogen is excrete in feces (gives feces its brown color)
20% of urobilinogen is reabsorbed, 10% of which is excreted in urine (gives urine its yellow color), other 90% re-enters the enterohepatic circulation
Differentiate sliding vs. paraesophageal hiatal hernia
Hiatal hernia = diaphragmatic hernia where stomach protrudes upwards thru esophageal hiatus
- sliding = GE jxn above esophageal hiatus
- paraesophageal = GE jxn is normal, but fundus of stomach herniates
Name the layers of the gut wall
‘MSMS’ from lumen outwards
- mucosa = epithelium, lamina propria, muscularis propria
- submucosa = secretes fluid, contains Meisner (submucosal) nerve plexus
- muscularis externa = motility (muscle), myenteric (Auerbach) plexus
- serosa when intraperitoneal (or adventitia when retroperitoneal)
How to differentiate esophageal atresia w/ and w/o tracheo-esophageal fistula
Both first diagnosable by trying to pass NG tube and it doesn’t enter stomach
W/o TEF => gasless abdomen (on CXR)
W/ TEF = gass in the abdomen
S/p episode of vomiting pt presents w/ this CT
(a) Dx
(b) Mgmt
(a) Dx = pneumomediastinum, given clinical scenario most likely 2/2 Boerrhave syndrome = transmural tear in esophagus from violent vomiting
(b) Mgmt = immediate surgery
Explain the arrowed finding
Stomach has a ‘cerebriform’ appearance (look like brain gyrae) b/c the rugae are so hypertrophied = gastric mucosa hyperplasia = Menetrier disease
- acquired premalignant condition of massive gastric folds
- increased risk of gastric adenocarcinoma
Name the organization of the femoral region
Lateral to medial: nerve, artery, vein, empty, lymphatics
‘venous to the penis’ = vein more medial
Name the borders of the anatomic triangle that direct inguinal hernias protrude through
Hasselbach (inguinal) triangle borders:
- medial border = lateral border of the rectus abdominis
- lateral border = inferior epigastric vessels
- inferior border = inguinal ligament
What are Brunner’s glands?
Brunner’s glands = duodenal glands (mark transition from stomach to duodenum)
Secrete HCO3- to:
- provide alkaline environment to activate intestinal enyzmes
- protect against acidity of chyme
Describe the mechanism of the two drugs used to decrease production of stomach acid
- PPI that directly inhibits the ATPase that pumps out H+ in exchange for K+
- H2 blocker = histamine receptor agonist to inhibit the main stimulatory signal of H+ production (histamine from ECL cells)
Label the branches of the abdominal aorta
- come out anteriorly if they supply the gut (celiac trunk, SMA, IMA)
- come out laterally if they supply non-gut structures (adrenal, renal, gonadal)
Celiac trunk out at T12 level, IMA at L3
What are portosystemic anastamoses
(a) Name the 3 major ones
Portosystemic anastamoses = connection btwn portal and systemic circulation
(a) 3 major:
- esophageal (left gastric and esophageal)
- caput medusae (paraumbilical recanalizes to small epigastric veins of anterior abd wall)
- anorectal varices (superior rectal to middle/inferior rectal a)
Label the branches of the celiac artery
Which are in the body of the stomach, antrum, duodenum?
(a) Parietal cells
(b) Mucus cells
(c) D cells
(d) K cells
(e) I cells
(f) Chief cells
(g) S cells
(h) G cells
(a) Parietal cells in the body of the stomach (secrete H+)
(b) Mucus cells (secrete bicarb/mucus) in antrum
(c) D cells in the antrum secrete somatostatin
(d) K cells in the duodenum secrete GIP (gastric inhibitory protein)
(e) I cells in the duodenum secrete CCK to stimulate pancreatic secretions
(f) Chief cells in the body of the stomach secrete pepsinogen
(g) S cells in the duodenum secrete secretin
(h) G cells in the antrum secrete gastrin (respond to vagus nerve)
Explain the concept of the alkaline tide post-prandially
Food in stomach stimulates gastrin secretion and H+ secretion, which in exchange pushes a bicarb into the serum
-basically pushing H+ into GI lumen creates an extra HCO3- that gets shuttled into the bloodstream to keep even charge inside the cell
So alkaline tide refers to a transient rise in pH often postprandially
-also seen in more severe form w/ vomitting where parietal cells compenstae for lost gastric acid creating huge alkaline tide and causing metabolic alkalosis
What are plicae circularis?
(a) Differentiate from gastric folds
(b) Differentiate from haustra
(c) Location
(d) Fxn
Plicae circularis = circular folds in the (c) jejunum and ileum of the small intestines
(a) Permanent, don’t disappear w/ distention like gastric folds
(b) Plicae circularis are circumferential (all the way around) while haustra are larger and don’t reach all the way around
(d) Increase surface area for absorption
Locate the site of a femoral hernia
Femoral hernias go thru the femoral ring = space btwn femoral vein and lymphatics (just medial to femoral vein)
Which zone of the liver is affected first by
(a) ischemia
(b) viral hepatitis
(c) Alcoholic hepatitis
(d) Metabolic toxins vs. exogenous toxins
Zone I = closest to arterial supply (portal triad)
Zone III = closest to ventral vein (most deoxygenated)
(a) Zone III
(b) Zone I
(c) Zone III
(d) Metabolic toxins first affect zone III, exogenous toxins (cocaine) first affect zone I
What are Peyer’s patches?
(a) Location- which layer?
(b) Fxn
= organized lymphoid follicules in the gut
(a) Distal SI (mostly ileum, some jejunum, few/rare duodenum). In submucosa layer and extend into mucosa layer
(b) Immune surveillance- contain macrophages, dendritic cells, B and T cells, trap foreign particles and surveillance and destroy them
Describe the 3 receptors on parietal cells that stimulate H+ secretion
- M3 (muscarinic) receptors that respond to ACh from vagus nerve
- Gastrin-responsive receptors directly responsive to gastrin
- H2 receptor stimulated by histamine from ECL cells (stimulated by gastrin)
- H2 receptor: G coupled protein to activate ATPase that pumps out H+ in exchange for a K+
Differentiate apical and basolateral membrane of hepatocytes
Basolateral membrane faces sinusoids
Apical membrane faces bile caliculi
Name the cutoffs of the embryologic
(a) Forgut
(b) Midgut
(c) Hindgut
(a) Forgut: pharynx to proximal 1/3 duodenum
- structures supplied by celiac artery
(b) Midgut: Duodenum to first 2/3 of transverse colon
- blood supply from SMA
(c) Hindgut: Distal 1/3 of transverse colon to anal canal above the pectinate line
- blood supply from IMA
Gastrochesis vs. omphalocele
Omplalocele- abdominal contents are covered by peritoneum, worse prognosis 2/2 associated cardiac defects
Gastrochesis- abdominal contents not covered by peritoneum
Differentiate the histologic appearance of the classes of lymphocytes
- Neutrophils = multilobed nucleus (2-5) w/ azurophilic lysosome granules
- monocytes (macrophage precursors) have large kidney-shaped nucleus w/ extensive “frosted glass cytoplasm”
- Macrophage
- Eosinophil = bilobate nucleus, eosinophilic granules of uniform size
- Basophil: densely basophilic granules containing heparin and histamine
What are Langerhans cells?
Langerhans cells = dendritic cells in the skin
-dendritic cells are highly phagocytic APCs, link the innate and adaptive immune system by expressing MHC class II and Fc receptors on surface
How to distinguish plasma cells on histology
“Clock face” chromatin distribution w/ abundant RER
-basically see clock-face appearance of nuclei
Name components of vascular endothelial cells that are
(a) Prothrombotic
(b) Anti-thrombotic
(c) Stabilize plt plug
Vascular endothelial cells have tons of stuff
(a) Prothrombotic = vWF (in alpha granules) and factor VIII
(b) Anti-thrombotic = PGI2 (prostacyclin = inhibits plt activation and vasodilates) and tPA
(c) Vascular endothelial cell contains thromboplastin that converts plasmiogen to plasmin so plasmin can stabilize fibrin clot (plasmin coverts fibrinogen to fibrin)
If you see an oval-shaped enlarged RBC on peripheral smear, what other blood cell abnormality would you expect to see?
Oval-shaped enlarged RBC = Macro-ovalocyte- seen in folate and B12 deficiency (megaloblastic macrocytic anemia) or bone marrow failure
-megaloblastic features involve enlargement of RBCs = macro-ovalocyte
Also exepct hypersegmented neutrophils
Give the etiology of basophilic stipling in the absence of anemia
Basophilic stipling = visualized ribosomes in cell periphery 2/2 defect in rRNA breakdown
- can occur b/c of regenerative anemias (both Fe deficiency and megaloblastic)
- w/o anemia: think of lead poisoning
Dx suggested by presence of the following cells on peripheral smear
Acanthocytes = spur cells = presence of abnormally spiked RBC membrane
-indicates dx of liver disease of abetalipoproteinemia (type of cholesterol dysregulation)
Name 4 conditions where the following cells are seen
Target cells = RBCs w/ excess membrane in the middle (interupting central pallor)
‘HALT to the target’
- HbC disease (glutamate –> lysine)
- Asplenia
- liver disease
- thalassemia
Type of RBC is most classically associated w/ what d/o?
Dacrocyte = ‘teardrop’ cell is classically indicative of myelofibrosis
- myelofibrosis = BM infiltrated and replaced by CT
- RBC is tugged to one end (creating tear drop shape) as it squeezes out of bone marrow or reticuloendothelial system w/ an increased amount of CT
Name 2 d/o w/ the following finding
Stimulation of hematopoesis outside the normal sites (usually confined to long bones) causes hyperplasia of skull and facial bone => crewcut appearance on Xray and chipmunk facies
-2/2 extramedullary hematopoiesis
Seen classically in: beta-thalassemia minor and sickle cell
Lab Values in iron deficiency anemia
Iron deficiency anemia: low serum Fe (duh), elevated TIBC/transferrin level (liver sees low iron so pumps out more transferrin)
-ferritin (stoarge) reduced
Lab values seen in anemia of chronic disease
Anemia of chronic disease: chronic inflammatory state = elevated inflammatory makers = elevated hepcidin sequesters iron away inside cells so it’s not accessible to RBCs for heme production
- elevated ferritin (b/c stores are high b/c can’t be accessed)
- low serum iron
- low transferrin saturation (none in blood)
- TIBC is reduced (always goes opposite of ferritin)
Lab values seen in sideroblastic anemia
Sideroblastic anemia = defective heme synthesis
- high ferritin (high stores b/c not being used)
- high serum iron and high TIBC (again high b/c not getting used)
- low TIBC (b/c always opposite ferritin)
Changes in TIBC and transferrin saturation seen in pregnancy and OCPs
- increaesd TIBC
- low percent saturation
Explain the mechanism of opioids
Opioids agonize the mu, delta, and kappa opioid receptors to (1) decrease synaptic nt release from presynaptic neuron (2) hyperpolarize postsynaptic neuron
-opioid binding to receptor => opens K+ and closes Ca2+ channels to reduce release of ACh, NE, 5-HT, glutamate, and substance P
Where do benzos and barbiturates work?
(a) What else works here?
Both benzos and barbiturates bind the GABA-A receptor (ligand-gated Cl- channel)
(a) Also bound by EtOH
but barbiturates increase duration of Cl- channel opening to reduce neuronal firing, while benzos increased frequency of Cl- channel opening (so duration vs. frequency)
Name two Parkinsons drugs that centrally inhibit DA degradation
Both COMT inhibitors (specifically Tolcopone works both peripherally and centrally) and MAO-B inhibitor Selegiline work centrally in presynaptic neuron to decrease DA degradation into
Mechanism of amantadine in use of Parkinsons tx
Amantadine (also antiviral) increases dopamine availability by increasing presynaptic DA release and inhibiting DA reuptake
Differentiate mechanism of tolcapone and entacpone
Both are COMT inhibitors that reduce degradation of DA (so useful as adjunct tx in Parkinsons d/o where DA is reduced)
But tolcapone works both centrally and peripherally, while Entacpone works only peripherally
-both used in ADJUNCT to L-DOPA (NOT ALONE)
Name the 4 pathways of dopaminergic transmission and explain their role in schizophrenia
4 main dopamine pathways
- Mesolimbic: VTA to nucleus accumbens, responsible for positive symptoms
- Mesocortical- VTA to prefrontal cortex repsonsible for negative symptoms
- Nigrostriatal- substantia nigra to striatum responsible for stimulation of purposeful movement
- Tuberoinfundibular pathway- DA pathways in hypothalmus from arcuate and periventricular nucleus to the infundibular region, responsible for inhibiting prolactin release
Dx
Dx = horseshoe kidney stuck lower in abdomen under root of the IMA
Explain the location of a horseshoe kidney
During development kidneys move from pelvis up into the abdomen, w/ lower poles fused the horseshoe kidney gets stuck at the root of the inferior mesenteric artery => doesn’t ascend fully so present in lower abdomen
Differentiate the three embryologic structures of the renal system
- Pronephros first- don’t do anything
- Mesonephros that act as kidneys for the first trimester, then go away or in males contribute to the GU system
- Metanephros are the permanent stuff that starts to form at the 5th week of gestation
Explain the etiology of a duplex collecting system
Duplex collecting system = two ureters for one kidney, increased risk VUR, ureteral obstruction, and UTI
Etiology is embryological: bifurcation of ureteric bud before it enters the metanephric blastema, or have 2 ureteric buds that reach the metanpehric blastema
What letter senses and responds to NaCl concentration
Macula densea (A)- specialized cells that line the thick ascending loop and lay btwn the afferent and efferent arteriole are sensitive to the NaCl concentration of incoming blood
-stimulate renin release if NaCl concentration drops
Relationship btwn ureter and vas deferens
“Water runs under the bridge” - ureter runs under both the uterine artery (females) and ductus deferens (males)
Ex: manipulation of uterine artery in the cardinal ligament during surgery can damage ureter => obstruction or leak
Differentiate the two components of the metanephros
Metanephros comprised of the ureteric bud and the metanpehric mesenchyme
Ureteric bud => ureter, pelvis, calyces, collecting ducts
Metanephric mesenchyme => nephrons
Differentiate activity of prostaglandins and ATII at the afferent and efferent arteriole
PGE preferentially vasodilate afferent arteriole => increasing both RBF and GRF so FF stays constant
ATII preferentially constricts the efferent arteriole which decreases RBF but increases GFR => increases FF
Percent of sodium reabsorbed in each part of the nephron
- Most (65-80%) reabsorbed in PCT
- thin descending loop impermeable to Na+
- thick ascending loop: 10-20% Na
- DCT: 5-10%
Where does Mg and Ca reabsorption get reabsorbed in the nephron?
Mg and Ca get reabsorbed in the thick ascending limb paracellularly (btwn the interstitial cells straight into blood)
-driven by positive lumen potential from K+ backleak
Action of aldo on the collecting tubule
Aldo
- upregulates ENac to increase Na reabsorption
- stimulates K+ secretion out into filtrate
- stimulates H+ ATPase => increase H+ secretion
Distinguish the two components of the JGA
Juxtaglomerular apparatus:
- Macula densa = cells of the DCT that sense NaCl concentration and moderate renin secretion
- JG cells = modified smooth muscle cells of the afferet arteriole that secrete renin
- Also includes mesangial cells
What cells release EPO
Interstitial cells in the peritubular capillary bed (arises from the efferent arteriole)
-renal peritubular interstitial cells
Function of Winter’s formula
Winter’s formula calculates the respiratory compensation expected for a simple metabolic acidosis
If the pt PCO2 is markedly different than the PCO2 calculated by Winter’s formula, then there is a second pH disturbance simultaneously occuring
pCO2 = 1.5 (HCO3) + 8 +/- 2
Where in the kidney is vitamin D activated?
25-OH vit D –> 1,25-OH vit D by 1 alpha hydroxylase in the PCT
-proximal convoluted tubule cells have 1 alpha hydroxylase
Benign renal tumor associated w/ large eosinophilic cells w/ abundant mitochondria
Renal oncocytom = benign renal epithelial cell tumor
Often surgically removed just to exclude RCC
Diuretic that
(a) Increases urine calcium
(b) Decreases urine calcium
and mechanism
(a) Loop diuretics increase urinary calcium excretion by reducing paracellular calcium reabsorption in PCT
(b) Thiazide diuretics increase calcium reabsorption by enhancing Ca reabsorption at the DCT
MC type of monozygotic twins
Most monozygotic twins cleave btwn 4-8 days, causing monochorionic, diamniotic twins
-so in two sacs (diamniotic) but one placenta (monochorionic)
Explain functional structure of the placenta
Fetal: cytotrophoblasts and syncytiotrophoblast line chorionic villi that protrude into lacunae (spaces filled w/ maternal blood).
Maternal artery from the decidua basalis (derived from endometrium) delivers blood into the decidua basalis
4 structures w/in the umbilical cord
Umbilical cord
1,2: two umbilical arteries returning de-O2 blood from fetal internal iliac arteries
3: single umbilical vein- delivers O2 blood to fetal IVC via ductus venosus or liver
4: allantoic duct = connects yolk sac and urogenital sinus, becomes the allantois that connects the fetal bladder and yolk sac
Differentiate urachal cyst from Meckel diverticulum
Both arise from failure of something connecting yolk sac to inside (either fetal bladder = urachus, or midgut lumen = vitelline duct) to obliterate fully
Urachal cyst = partial failure of urachus to obliterate => fluid-filled cavity lined w/ uroepithelium btwn umbilicus and bladder
Meckel diverticulum = partial closure of vitelline duct w/ open portion to instestinal lumen
Derivatives from the 6 aortic arches
1st arch- maxillary artery (end branch of external carotid artery)
2nd arch- Stapedial artery and hyoid artery
3rd (C is the 3rd letter)- common carotid artery, proximal part of internal carotid artery
4th- aortic arch on left, proximal R. subclavian on R
6th- proximal part of pulmonary arteries and ductus arteriosus
Structures derived from the 4 brachial pouches
Brachial pouches (‘CAP’) are from endoderm
1st pouch- middle ear cavity
2nd pouch- tonsillar lining
3rd pouch- thymus and inferior parathyroids (ironically 3rd pouch structures end up below 4th pouch structures)
4th pouch- superior parathyroids
Mesonephric vs. paramesonephric duct
Females: mesonpehric duct degenerates, paramesonpehric –> internal female genitalia (fallopian tubes, uterus, upper vagina)
Males: paramesonephric degenerates, mesonephric duct –> seminiferous tubules, epididmyis, ejaculatory duct, ductus deferens
Function of SRY gene
SRY gene on male chromosome codes for testes-dermining factor for testes development
Testes need to develop so there are sertoli and leydig cells present to produce mullerian inhibitory factor and testosterone respectively
Male equivalent of
(a) Glans cliteris
(b) Labia minora
(c) Labia majora
(d) Bartholin glands
Male equivalent
(a) Clitoris = glans penis (from genital tubercle)
(b) Labia minora = ventral shaft of penis (from urogenital folds)
(c) Labia majora = scrotum (from labioscrotal swelling)
(d) Bartholin glands = Bulbourethral glands of Cowper
Function of the infundibulopelvic (suspensatory) ligament of the ovary
(a) Vessels contained
Suspensatory ligament attaches the ovary to the lateral pelvic wall
(a) Contains ovarian vessles (artery and vein) that need to be ligated during oophorectomy
Functional of the cardinal ligament
(a) BV contained
Cardinal ligament attaches the cervix to the side wall of the pelvis
(a) Contains the uterine vessels
Round ligament of uterus
(a) Fxn
(b) Remnant
Round ligament of the uterus connects the fundus to the labia majora- goes down thru round inguinal canal to continue downwards
Function of broad ligament
Broad ligament attaches the fallopian tube, ovary, and uterus both to each other and to the pelvic wall
MC location of cervical cancer
Cervical transformation zone = transition btwn stratified squamous of ectocervix and simple columnar of endocervix
- very distinct border, literally can be one cell thick
- this transformation zone is the MC location of cancer, and is what we sample w/ pap smear
Pathway of sperm for ejaculation
SEVEN UP
Seminiferous tubules
Epididymis
Vas deferens
Ejaculatory duct
nothing
Urethra
Penis
Describe the anatomy of the seminiferous tubule
(a) Location of cells
(b) Location of blood supply
So capillaries and Interstitial cells of Leydig (stimulated by LH to release testosterone) are in the intersitium
Then spermagonia line the seminiferous tubueles and are surrounded by supporting Sertoli cells (stimulated by FSH to release inhibin)
Explain the interaction btwn the two supporting cells in the ovary that leads to estrogen production
LH stimulates theca cells to convert cholesterol to androgens, then androgens from theca cells are taken up by granulosa cells
Granulosa cells stimualted by FSH to convert androgens to estrogens
Estrogen formed in the ovary = estradiol which is the most potent (more potent than estrone from peripheral fat and estriol from placenta)
Explain when oocytes undergo each part of meiosis I and II
Primary oocyte starts meiosis I during fetal life
-meiosis I arrested in prOphase I for years until Ovulation
Then meiosis II is arrested in METalphase II until fertilization (sperm MET egg) = secondary oocyte
If fertilization doesn’t occur, secondary oocyte degenerates before finishing meiosis II a
Blood hormones that cause ovulation
Get peak in estrogen that causes LH surge from anterior pituitary, LH surge causes rupture of follicle (ovulation)
After ovulation start to see progesterone rise b/c corpus luteum produced from leftover granulosa and theca cells in ovary
Spermatid vs. Spermatogonium vs. Speratozoon
Speratogonium: dipoid gamete cell before meiosis has even started
“gonium is eventually going to be sperm”
Spermatogonium –> primary spermatocyte (diploid) –> secondary spermatocyte (haplod) –> haploid spermatid
Spermiogenesis converts haploid spermatid to mature spermatozoon (“zoon is zooming to egg”) by adding acrosome
Differentiate placenta accreta/increta/percreta
Defective decidual layer causes abnormal attachment of placenta to myometrium
Placenta accreta = placenta attaches to the myometrium w/o penetrating it (MC type)
Placenta increa = placenta penetrates into myometrium
Placenta percreta (most severe)- placenta penetrates into myometrium and into uterine serosa- so invades entire uterine wall, can even cause placental attachment to rectum or bladder
What is vasa previa?
(a) Association w/ velamentous umbilical cord insertion
Vasa previa = when the fetal vessels run over the cervical os
- can cause painless vaginal bleeding w/ fetal bradycardia (under 110 bpm), usually indicates emergency C-sxn
(a) Velamentous umbilical cord = cord inserts in chorioamniotic membrane rather than the placenta => the fetal vessels travel to the placenta unprotected by Wharton jelly
Name 2 benign tumors of breast stroma
Breast stroma tumors
- Fibroadenoma = MC tumor in F under 35, size and tenderness fluctuates w/ estrogen exposure, not a precursor to breast cancer
- Phylloides tumor = bulky mass of CT w/ ‘leaf like’ projection
- may become malignant
Use of Leuprolide
Leuprolide = GnRH analog (synthetic GnRH)
- can give in pulsatile fashion to stimulate anterior pituitary: used in infertility
- can give continuously to inhibit anterior pituitary: used in prostate cancer, uterine fibroids, precocious puberty
3 feedbacks on NE release from presynaptic terminal
- ATII increases NE release
- Alpha-2 innervation inhibits NE release
- NE itself exerts negative feedback, acts on presynaptic alpha 2 to decrease NE release
Explain effect of NE on
(a) BP
(b) HR
NE- think primarily alpha1 agonist
(a) Increases MAP w/ no change in pulse pressure b/c increase is in both systolic and diastolic (from alpha1 mediated vasoconstriction)
(b) Reflex bradycardia
- alpha1 mediated increase in BP => reduced HR from reflexive beta tone from carotid body
Effect of isoproterenol on
(a) BP
(b) HR
Isoproterenol = equal beta 1 and beta 2 agonist, no alpha
(a) Decrease in MAP w/ increase in pulse pressure
- beta2 mediated vasodilation reduces MAP, diastolic reduced more then systolic
(b) HR increased thru beta1 chronotropy
Change in BP when high Epi is on board and Phentolamine is administered
High dose epi is mostly alpha w/ some beta, alpha1 predominates. So see increase (net pressor effect) before alpha blockade (Phentolamine) given
-then when phentolamine is given beta2 activity of Epi is uninhibited => see reversal in BP change, now net depressor effect of epi
Differentiate zero and first order kinetics
Zero-order elimination = constant rate of elimination, doesn’t depend on concentration
1st order = constant fraction of the drug eliminated per unit time, so elimination directly correlates w/ drug concentraiton
Formula for therapeutic index
TI = TD50 / ED50
TD50 - median toxic dose
ED50 = medium effective dose
Wider the TI = easier drug is to dose and prevent side effects, more wiggle room
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