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BECOM 2 > BECOM Exam #4 > Flashcards

BECOM Exam #4 Flashcards

1
Q

Pituitary part names

A 
Ant: pars distalis
Post: pars nervosa
pas intermedia (in between ant and post)
infundibular stalk
pars tubulars (surrounds infundibular stalk)
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2
Q

Posterior innervation and secretion (from hypothalamus)

A

paraventricular nucleus: oxytocin

supraoptic nucleus: ADH

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3
Q

Anterior communication with hypothalamus

A

hypophyseal portal vein

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4
Q

Hypophyseal pouch ectoderm forms

A

ant pituitary

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5
Q

Neurohpoyseal pouch neuroectoderm forms

A

post pituitary

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6
Q

anterior pituitary cells and function (acidophils and basophils)

A
  • Acidophils – contain polypeptide hormones
    1. Somatotrophs – secrete growth hormone (GH, aka somatotropin)
    2. Mammotrophs (aka Lactotrophs) – secrete prolactin (PRL)
  • Basophils – contain glycoprotein hormones
    1. Gonadotrophs – secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH)
    2. Thyrotrophs – secrete thyrotropin (TSH)
    3. Corticotrophs – secrete adrenal corticotropin (ACTH) and lipotropin (LPH)
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7
Q

Pars intermedia cell type

A

corticotrophs

chromotrophs

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8
Q

Pars Tubularis cell type

A

gonadotrophs

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9
Q

Pituitary adenomas types (cell types and hormone)
gigantism
loss of mensural cycle
Cushing disease

A

gigantism: somatotrohs -> GH
loss of mensural cycle: lactotrophs -> prolactin
Cushing disease: thyrotrophs -> hyperthyroidism

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10
Q

Thyroid cell type and hormone

A 
Follicular cell (thyocyte): thyroglobulin
Parafollicular cells (c cells): calcitonin
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11
Q

parathyroid cell type and hormone

A

principal cells: parathyroid hormone (PTH)

oxyphil cells: some PTH but mainly nonfunctional

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12
Q

Adrenal Cortex layers and steroids

A
  • capsule
  • zona glomerulosa: mineralcoticoids (aldosterone)
  • zona fasciculata: glucocorticoids (cortisol)
  • zona recticularis: dehydroepiandrosterone DHEA a precursor to testosterone
  • adrenal medulla: epinephrine and norepinephrine
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13
Q

Addison’s disease

A

destruction of particular cell type of adrenal cortex

-KNOW layers and correlate to different symptoms of Addison’s disease

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14
Q

Pineal Gland contents and release

A

corpus arenaceum (brain) sand: releases melatonin

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15
Q

POMC

A

POMC is cleaved into

  • ACTH and B-lipoprotein (B-LPS)
  • ACTH contain alpha-MSH
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16
Q

Pregnancy can cause infarction in the pituitary

A

d

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17
Q

Serous inflammation

A

Excess watery fluid exudate…blisters

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18
Q

Serofibrinous inflammation

A

Exudate rich in fibrin

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19
Q

Catarrhal inflammation

A

Mild inflammation of mucous membrane with excess watery secretion

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20
Q

acid fast pos. gastrointestinal protozoa

A

Cryptosporidia, Cyclospora

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21
Q

Giardiasis

A

Causative agent: Giardia lamblia
Manisfestations: sulfurous belching/flatulence, fat-rich stools, diarrhea and vomiting
-#1 protozoan intestinal disease in US
-contaminated water, after someone goes camping (beavers)

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22
Q

Cryptosporidium

A

Causative agent: Cryptosporidium parvum
Manisfestations: self-limiting watery diarrhea in immunocompetent hosts (AIDS) will run course in normal individual
-epidemic community diarrhea outbreaks
-ACID-FAST positive

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23
Q

Cyclospora

A

Similar manifestations as cryptosporidium but larger histologically
-ACID-FAST positive

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24
Q

Amebiasis

A

Causative agent: Entamoeba histolytica
Manisfestations: amoebic dysentery (traveler’s dysentery)
-histologically will contain RBCs within

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25
Q

toxoplasma gondii

A

CAT POOP parasite

  • can also be found it uncooked meat or unwashed vegetables
  • can affect pregnant women fetus
  • lesion scattered across brain in immunocompromised individuals
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26
Q

Acanthamoeba

A
  • effects eye usually through effected contacts

- found in USA

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27
Q

Naegleria fowleri

A

Disease: Rapidly fatal primary amoebic meningoencephalitis by amoeba borrowing through cribriform plate into brain
Transmission: swimming in freshwater lake
Diagnosis: Amoebas in spinal fluid
-found in USA

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28
Q

trypansoma brucii

A 
Disease: African Sleeping Sickness
Manifestation: characterized mainly by sleeping problems insomnia or sleepiness
Transmission: Tsetse fly (painful bite)
Diagnosis: Trypomastigote in blood smear
-AFRICA
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29
Q

plasmodium

A

P. falciparum
P. malariae (Anopheles mosquitoes)
P. vivax
P. ovale

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30
Q

plasmodium falciparum

A

Manifestation: cerebral hemorrhaging and blood in urine (lyses 10% of blood cells)
Diagnosis: produces banana shaped

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31
Q

babesiosis

A

Manifestation: fever and hemolytic anemia:
Transmission: US tickborne illness
Diagnosis: Maltese Cross on histological slide

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32
Q

Trichomonas vaginalis

A

Manifestation: foul-smelling greenish discharge
Transmission: sexual
Diagnosis: Motile ‘pear-shaped’ trophozoites and strawberry cervix

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33
Q

leishanosma spp

A

Disease: Visceral leishmaniasis (fatal) or Cutaneous leishmaniasis
Transmission: Sandfly
Diagnosis: Macrophages with amastigotes

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34
Q

trypanosma cruzi

A

Disease: cardiomegaly, megacolon, and megaesophagus (Chagas Disease) or unilateral periorbital swelling
Transmission: kissing bug
Diagnosis: Trypomastigote in blood smear

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35
Q

mites vs lice

A

mites, scabies, and chiggers: burrow

lice: don’t jump, close contact

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36
Q

17alpha hydroxylase def

A
  • will have a decrease in hydroxylase not a complete loss of hydroxylase
  • normal levels of aldosterone but decreased DHEA and cortisol
  • low cortisol -> no neg feedback on ACTH -> increase pigmentation
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37
Q

21 hydroxylase (CYP21A2) def

A
  • normal levels of DHEA and aldosterone but low cortisol levels
  • KEY LOW 11-deoxycortisol
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38
Q

11 B hydroxylase (CYP11B1) def

A
  • normal levels of DHEA and aldosterone but low cortisol levels
  • KEY HIGH 11-deoxycortisol
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39
Q

aldosterone vs cortisol binding to albumin and CBG

A

cortisol has a higher affinity for CBG than aldosterone

-inc cortisol will unbind aldosterone from CBG increasing blood aldosterone levels

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40
Q

Side effects of aldosterone excess

A
  • High salt intake suppresses the angiotensin system and can lead to shrinkage of the zona glomerulosa
  • high Na+
  • alkalosis (H+ secretion)
  • low K+
  • Promote inflammation and fibrosis in cardiovascular system
  • Systolic and diastolic dysfunction
  • damaging effects on the cardiovascular system, baroreceptors and kidneys and can lead to worsening heart failure
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41
Q

Aldosterone escape

A

Aldosterone increase -> increase in Na+ retention -> transient increase in arterial BP -> pressure diuresis and increased ANP secretion (natriuresis)

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42
Q

Cortisol metabolic functions

A
  • inc glucose
  • dec insulin sensitiivity
  • inc lypolysis
  • dec protein synthesis (inc protein catabolism)
  • Inhibit keratinocyte proliferation and collagen synthesis
  • Promote osteoclast activity
  • Postpartum cortisol is needed for initiation of lactation by PRL
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43
Q

Cushing Disease

A
  • excessive glucocorticoids
  • striae (stretch marks) - inhibition of collagen synthesis
  • Osteoporosis - promotion of osteoclast activity
  • Hypertension - alpha receptor epi and NE, NA+ retention
  • Disturbance in menstrual cycle
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44
Q

Tg time in the follicle

A

the longer in follicle more time for iodine to be added by TPO resulting in more T4, if in follicle for less time (during increase demand) less iodine added by TPO resulting in more T3

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45
Q

T3 vs T4

A

T3: active
T4: inactive

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46
Q

DIT and MIT

A

are recycled to Tyrosine and I- by iodotyrosine deiodinase (transported to the follicular lumen by Pendrin)
-Iodine def. without DIT and MIT cant reclycle iodine, a lot of iodine in urine

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47
Q

Selenodeionidases (D1 vs D2 vs D3)

A

D1: T4 -> T3 (liver, kidneys and thyroid tissue)
D2: T4 -> T3 (CNS)
D3: inactivates T3 to DIT and T4 to RT3

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48
Q

Goiter syndrome

A

-is an enlargement of the thyroid gland in the neck
Causes:
-low iodine -> low T3 -> no negative feedback
-

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49
Q

T3 function

A
  • Stimulate the pituitary somatotrophs to express GH and increases IGF-1 in bones and muscles (INDIRECT)
  • Direct stimulatory role on bones and muscle tissues (↑ synthesis of enzymatic and structural proteins) (DIRECT)
  • inc BMR (increases oxidative respiration capacity, UCP-1)
  • Inc B1 adrenergic receptors -> inc HR
  • INC GLUCOCORTICOID INACTIVATION -> INC ACTH
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50
Q

T3 and T4 function (nuclear)

A

-Nuclear activation and non classical activation of membrane receptor (both T3 and T4) -> synthesis of new proteins

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51
Q

Giant Cell

A

multinucleated cells that form as a result of Granulomatous Inflammation

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52
Q

Caseating granuloma vs Noncaseating granulomas

A

Caseating: focus of activated macrophages (epithelioid cells), rimmed by fibroblasts, lymphocytes, histiocytes, occasional Langhans giant cells; central necrosis with amorphous granular debris; acid-fast bacilli
-central zone: necrotic, granular, “cheesy” appearance

Noncaseating: granulomas with abundant activated macrophages
-central zone: non-necrotic

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53
Q

vitamin D activation

A

Cholecalciferol -> 25-hydroxycholecalciferol –(PTH)–> 1,25-dihydroxycholecaliferol

high calcium or low PTH decrease 25-hydroxycholecalciferol -> 1,25-dihydroxycholecaliferol

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54
Q

Vitamin D actions

A

↑ intestinal calbindin  ↑Ca++ absorption
↑ Ca++-dependent ATPase and alkaline phosphatase
↑ phosphate flux through the intestinal epithelium
↑ Ca++ and phosphate renal secretion (minimal effect)

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55
Q

b cells:
a cells:
d cells:

A

b cells: secrete amylin (dec gastric emptying, dec glucagon secretion) and insulin
a cells: secrete glucagon
d cells: secrete somatostatin
F cell: secrete pancreatic polypeptide (PP)
e cells: secrete gherlin

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56
Q

GLP-1, GIP and CCK (incretins)

A
  • primes the b cells for the incoming hyperglycemia
  • GLP-1 surpasses glucagon
  • Dipeptidyl peptidase IV inhibitors increase GLP-1 and improve glucose tolerance
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57
Q

tyrosine-phosphatases (PTP)

A

terminates insulin receptor signaling

  • ex. PTP1B and leucocyte antigen-related (LAR) phosphatase
  • over expression in patients with insulin resistant diabetes
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58
Q

stress affect on ACTH

A
  • stress increase CRH -> increases ACTH
  • chronic stress can result in in constantly elevated threshold for the glucocorticoid negative-feedback mechanism (requires higher cortisol levels to decrease CRH and ACTH)
  • HYPOGLYCEMIA is a stress signal which causes CRH release
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59
Q

Diurnal variation and ACTH

A
  • CRH and ACTH are normally released in a pulsatile fashion
  • CRH and ACTH will be higher earlier in the morning because of low levels glucose
  • Lower levels of CRH and ACTH in the day time
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60
Q

Metabolic (direct) actions of GH

A
  • metabolizes lipids, carbohydrates (inc FA oxidation)
  • increase insulin resistance
  • ↑ thyroid secretion
  • ↑ fasting glucose levels by ↑ hepatic glycogenolysis and gluconeogenesis
  • ↓ and amino acid protein catabolism and inc protein synthesis
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61
Q

Anabolic actions of GH

A

through IGF-I/somatomedin (INDIRECT)

  • GH stimulated growth through IGF-1/somatomedin (INDIRECT)
  • bone growth
  • protein synthesis (muscle growth)
  • form somatomedin C which has a longer half life than GH
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62
Q

IGF-1

A
  • bone growth
  • muscle growth (inc AA uptake and inc protein synth)
  • cartilage growth
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63
Q

Gigantism

A

high GH before epiphyseal closure

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64
Q

Acromegaly

A

high GH after epiphyseal closure -> disproportionate growth

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65
Q

Symptoms and signs of GH excess

A
  • Musculoskeletal (protruded mandible, enlarged forehead, pressure-induced osteoarthritis, large hands and feet with square fingers)
  • Cardiovascular (Dilated cardiomyopathy, cardiomegaly, CHF)
  • Metabolic (high glucose, dec insulin sensitivity (diabetes))
  • Elevated IGF-I
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66
Q

High ADH (SIADHS)

A
  • Hyponatremia (increase volume -> release ANP -> secrete Na+)
  • Concentrated urine
  • Elevated urinary Na
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67
Q

StAR

A

after cholesterol ester is cleaved by cholesterol esterase StAR is used to transport cholesterol across the mitochondrial membrane so steroidogenesis can occur

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68
Q

Zona glomerulosa

A
  • lacks CYP17A1 (17a-hydroxylase) and cannot produce DHEA or glucocorticoids
  • aldosterone production
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69
Q

Primary hyperaldosteronism vs Secondary hyperaldosteronism

A

Primary hyperaldosteronism: adrenal tumor

Secondary hyperaldosteronism: high activity of the renin-angiotensin system

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70
Q

pregnancy effect on CBG

A

increase CBG which will increase total T3/T4 but normal T3/T4 blood levels

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71
Q

In long term cortisol excess

A
  • increased adipocytes differentiation (centripetal obesity)

- increase cortisol neg feedback threshold

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72
Q

oxytocin during development

A

cardiomyocytes and neural development

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73
Q

cortisol during development

A

Lung maturation

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74
Q

Dehydroepiandrosterone (DHEA)

A

-Responsible for adrenarche (early stage sexual maturation) before or around puberty in male and female

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75
Q

Dehydroepiandrosterone (DHEA) during pregnancy

A

In placenta, 16a-OH-DHEA is converted to 16a-OH-androstenedione and then to estriol (E3)

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76
Q

Adrenogenital syndrome
adult females
newborn females
prepubertal males

A

adult females: deep voice, large muscles, fascial hair, breast become smaller
newborn females: partially male-type external genitalia
prepubertal males: Precocious pseudopuberty

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77
Q

TPO activity is stimulated by

A

Stimulated

  • TSH (which also increases NIS, follicular cell proliferation and Tg endocytosis)
  • hCG of pregnancy
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78
Q

hCG

A

mimics TSH on follicular thyroid cells

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79
Q

T3 during development

A

neonatal brain development

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80
Q

Metabolic actions of thyroid hormones

A

↑Glucose absorption from the intestine
↑Glycolysis, gluconeogenesis and oxidative phosphorylation
↑Lipolysis, ↑ LDL  ↓ plasma cholesterol
↑Protein synthesis and degradation (net effect is catabolic)

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81
Q

Thyroid actions on cardiovascular system

A
  • inc cardiac output (also due to increased b adrenergic receptors
  • inc pulse pressure
  • inc a myosin heavy chain -> in the speed of cardiac contractions
  • inc Sarcoplasmic reticulum Ca++ ATPase
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82
Q

JAK/STAT

A

GH and prolactin

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83
Q

somatomedin C

A

IGF-I

longer half-life than GH

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84
Q

PC1/3

A

clips out of the c peptide (proinsulin -> insulin) and cleaves POMC????????????

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85
Q

PTH-related peptide

A

can be released by tumors and have nothing to do with the parathyroid causing hypercalemia

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86
Q

low dose Vitamin D vs high dose

A

Small quantities -> promotes bone calcification

Extreme dose of Vit D -> bone resorption

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87
Q

paid PTH effect
slow PTH effect

other effect:

A

paid PTH effect:
-Ca2+ pump at osteolytic membrane (Ca2+ from bone to ECF)
slow PTH effect:
-inc RANKL and M-CSF secretion from osteoblasts that increases osteoclast
-suppress OPG which will dec osteoblast

other

  • ↑ Ca++ reabsorption (TRPV5) at nephron
  • ↑ phosphate loss
  • ↑ the absorption of Mg++
  • ↑ 1,25-dihdroxycolecalciferol which increases intestinal Ca2+ reabsorption
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88
Q

excessive Ca2+

A

decrease parathyroid size
-High Ca++ -> stimulation of Ca++ sensing receptor/CaSR (G-coupled protein) -> activation of IP3, DAG and intracellular Ca++ -> ↓ PTH secretion

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89
Q

Calcitonin

A
  • produced by C cells of thyroid gland
  • Secreted in response to increase in plasma Ca++ concentration
  • Acts to lower plasma Ca++ levels by inhibiting activity of bone osteoclasts
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90
Q

PTH hypersecretion

A
  • hypercalcemia (causes hyporeflexia and muscle weakness)
  • hyperphosphaturia (bc osteoclast inc alkaline phosphatase)
  • renal stones
  • bone decalcification
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91
Q

PTH hyposecretion

A

-hypocalcemia (causes hyperreflexia and tetany)
-hyperphosphatemia
-

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92
Q

Vitamin D deficiency

A

soft bones (rickets and osteomalacia) bc getting Ca2+ from bones

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93
Q

amylin

A
  • reduces gastric emptying (satiety)

- inhibits glucagon

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94
Q

somatostatin

A
  • inhibits secretion of insulin, glucagon, and pancreatic peptide
  • stimulate glucose and amino acid ingestion
  • reduce GI motility
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95
Q

sulfonylurea

A

blocks K+ channel on pancreatic B cells causing depolarization and insulin release

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96
Q

finsulin promotes

A
  • glycogen synthesis
  • glycolysis
  • lipogenesis (dec ketone bodies)
  • protein synthesis
  • Increases GLUT4 expression
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97
Q

moderate exercise vs. intense exercise vs. stress

A
  • moderate exercise: proportional glucose uptake and glucose production bc GLUT4 stimulated by exercise is equal to catecholamine lipid and glucose production
  • intense exercise: more glucose production than glucose uptake (hyperglycemia) bc high catecholamine release (inc glucose and lipolysis) while also suppressing GLUT4 by inhibiting insulin secretion
    stress: high glucose production and little glucose uptake (can cause insulin resistance diabetes) bc catecholamines are suppressing insulin secretion while increasing blood glucose
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98
Q

glucagon stimulated by and increases

A

Hypoglycemia
Increased amino acids
Norepinephrine
Epinephrine

↑ hepatic glycogenolysis
Gluconeogenesis
Lipolysis

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99
Q

how does oxytocin cause contraction

A

PLC and PKC cause inc Ca2+ -> contraction

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100
Q

Leydig cell function

A

release testosterone into blood vessels and seminiferous tubules

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101
Q

Sertoli cell function

A
  • nourish germ cells
  • movement of germ cells
  • structural support
  • blood testis barrier (immunological privileged site due to tight junctions)
  • secrete androgen binding protein (binds testosterone in seminiferous tubule to allow spermatogenesis FSH DEPENDENT)
  • secrete inhibit (inhibits FSH when testosterone levels are hit)
  • phagocytize (residual bodies and degenerated cells)
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102
Q

Cryptorchidism

A

when the testis don’t descend and temp is 37-38 which won’t allow spermatogenesis to occur

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103
Q

Spermatogonial Phase

A

Type A dark: resident processor cell
Type A pale: divide into type B cell
Type B: differentiate into spermatocyte

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104
Q

Spermatocyte Phase

A

Primary spermatocyte: meiosis I, large cell

Secondary spermatocyte: meiosis II, smaller cell

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105
Q

Spermiogenesis Phase

A
  • Golgi Phase: form proacrosomal granules, centrioles migrate, axoneme formation (core of flagellum)
  • Cap Phase: acrosomal cap formed
  • Acrosome Phase: machete formed and mitochondria migrate posteriorly
  • Maturation Phase: residual bodies formed
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106
Q

Chemical Mediators (PAMPs and corresponding receptors)

A 
Endotoxin				TLR4
Lipoproteins			        TLR1, 2, 6
Peptidoglycan			NOD 1 & 2
Heat shock proteins		TLR2 and 4
Bacterial DNA			TLR9
Bacterial RNA			        TLR3, TLR7, TLR8
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107
Q

Chemical Mediators (DAMPS and corresponding receptors)

A

High Mobility Group box 1 RAGE, TLR2, TLR4, TLR7/8,TLR9, IL-1R, or CXCR4
Heat shock proteins TLR2, TLR4 in a CD14 dependent fashion
RNA and DNA TLR3, TLR7, TLR8, TLR9
Mitochondria TLR9
ATP varied, amplify effects LPS, IL-1b and IL-18
S100A8/S100A9 TLR3 trafficking and function
Heme induces TNF-a via NFkB pathway

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108
Q

Extravation

A
  • leakage of leukocytes form capillaries into infected/damaged tissue
    margination: leukocytes adhere to blood vessel wall (INTEGRINS on leukocytes and ICAM/SELECTIN on endothelial cell)
    diapedesis: leukocytes squeeze between endothelial cells into tissue
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109
Q

IL-1B, IL-6, TNF-a

A

cytokines that signal for acute phase proteins (mainly IL-6), neutrophil mobilization, increase body temp

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110
Q

acute phase proteins and purpose

A

C-reactive protein (opsonization)
mannose-binding lectin
fibrinogen (clotting factor)

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111
Q 
Chemokines attract what cell
CXCL8
CXCL7
CCL3
CCL5
CXCL-1
A

CXCL8: neutrophils, naive T cells
CXCL7: neutrophils
CCL3: monocytes, NK and T cells, basophils, dendritic cells
CCL5: monocytes, NK and T cells, basophils, eosinophils, dendritic cells
CXCL-1: neutrophils, naive T cells, fibroblasts

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112
Q

Transudate edema

A

extravascular fluid with low protein content

-due to increase hydrostatic pressure

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113
Q

Exudate edema

A

mast of cells and fluid seeping out of blood vessels

-due to increase vascular permeability

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114
Q

Suppurative (Purulent) vs Non-Suppurative

A

Suppurative: severe acute inflammation with pus
-pyogenic bacteria
-localized
Non-Suppurative: acute inflammation with less proteins
-Serous (blister)
-Serofibrinous (rich in fibrin)
-Catarrhal (irritation of mucous membrane plus watery secretion)
-Pseudomembranous inflammation (Diptheria and Shigella endotoxins)
-Hemorrhagic inflammation
-Necrotizing inflammation
-Allergic inflammation

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115
Q

mesonephric duct forms

A

f

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116
Q

Amoebic vs Bacterial Dysentery

A

Amoebic: Entamoeba histolytica
-variable fever
Bacterial: Shigella spp
-high fever

BOTH will have fecal leukocytes

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117
Q

Classical vs. Alternative Macrophage actions

A

Classical: Th1 produces IFN-y to activate macrophage resulting in the release of ROS, NO and lysosomal enzymes to kill infectious agent. Chemokines and cytokines are release to cause inflammation
Alternative: Th2 release IL-4/IL-13 which causes macrophage to release growth factors/TGF-B which will cause tissue repair/fibrosis and IL-10/TGF-B which will cause anti inflammation

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118
Q

Importance of LH surge

A
  • Caused by high levels of E2
  • High E2 stimulates Kiss peptide secreting hormones and anterior pituitary cells
  • It causes increase in PA and other proteases -> inc collagenase
  • Exits the egg from1st meiotic arrest (indirect)
  • Induces smooth muscles contraction
  • Within 2 h -> increased progesterone
  • Hypertrophy of GC -> luteinization
  • Increased prostaglandin and histamine in the dominant follicle -> hyperemia
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119
Q

NSAIDs effect on menstrual period?

A

cause heavier bleeding bc blood is thinner and prostaglandin is inhibited causing no uterine contractions (help expel blood and debri)

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120
Q

fibrinolysin

A

prevent menstrual blood from coagulating

-Heavy menstrual cycle will have clots bc little fibrinolysin

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121
Q

collegenase

A

high during LH surge allowing ovulation of egg

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122
Q

cervical mucous (estrogen and progesterone)

A
  • estrogen levels makes the mucous thin and watery

- progesterone in the second half of the cycle causes the plug to be thick and impenetrable by the sperms

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123
Q

Menopause

A
  • Hot flashes are caused by loss of vasomotor tone (temporary disturbances in hypothalamic thermoregulation)
  • Elevated gonadotropins in blood (mainly FSH)
  • Risk of osteoporosis and cardiovascular diseases increase after menopause
  • Irritability, fatigue, anxiety and decreased strength are often associated with menopause
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124
Q

high androgens and infertility

A
  • Testosterone is converted into DHT and DHT inhibits aromatase (no testosterone -> estrogen)
  • No negative feed back by estrogen on GnRH so high LH and high testosterone loop
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125
Q

Female reproductive tract aids in sperm migration

A
  • Contractions of myometrium propels the sperms toward the oviducts
  • Progesterone relaxes the ovarian ducts -> allow the passage of the morula
  • Upward contractions of oviduct smooth muscle
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126
Q

Zona reaction

A

Release of cortical oocyte granules causes oocyte membrane to become impenetrable to other sperm

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127
Q

Progesterone functions after fertilization

A
  • Prime the uterus for implantation (decidualization)
  • Inhibits myometrium contractions while estrogen stimulates the contractions
  • Progesterone in fetus is converted to DHEAs which flows back to placenta to be converted to estriol (E3 weakest estrongen but large amount)
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128
Q

respiration rate during pregnancy and result

A

Icn bicarb in pregnant women urine bc inc CO2 exhalation causing respiratory alkalosis, kidney will secrete bicarb in response

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129
Q

Human Chorionic gonadotropin (hCG) (placenta hormone)

A
  • Binds the same receptor as LH
  • Sustains the corpus luteum during the first 6-7 weeks of pregnancy
  • hCG also lowers the uterine contractility and support sexual development in male fetus
  • hCG has TSH-like activity  increases thyroid synthesis and albumin levels
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130
Q

Human chorionic somatomammotropin (placenta hormone)

A
  • mix between GH and prolactin
  • Increases the mother’s sugar level by promoting glycogenolysis and blocking glucose uptake (similar to GH actions) by reducing insulin sensitivity
131
Q

Estrogen (Estriol/E3) (placenta hormone)

A
  • The weakest estrogen
  • Formed primarily from fetal DHEA
  • Stimulates breast growth and duct growth (hyperplasia)
  • Stimulates proliferation of uterine muscle cells, increases their oxytocin receptors and gap junctions
  • uterine contraction
  • Similar to aldosterone (inc Na+ reabsorption)
132
Q

Progesterone (placenta hormone)

A
  • inhibit the estrogen actions on the uterine smooth muscle contractions
  • Inhibits the milk secretion
  • Is converted into other steroids
  • Towards the end of pregnancy, the fetal cortisol (and surfactant) causes more E3 to be made from this progesterone therefore favoring uterine contractions
133
Q

Insulin (fetal hormone)

A
  • Increased in response to excess maternal glucose

- In uncontrolled diabetic mothers, increased insulin has anabolic effects on the fetus -> oversized newborn

134
Q

androgen in regulating GnRH pulsatility

A
  • inhibition of GnRH pulse frequency is antagonized by androgens
  • dec LH and FSH
  • Testosterone has a direct inhibition effect on GnRH
135
Q

stress effect on GnRH

A

CRH, ADH, ACTH, endogenous opioid peptides (e.g., β-endorphin), and cortisol surpasses GnRH

136
Q

what determines the half life of a hormone

A

amount of glycosylation

-FSH has longer half-life in circulation than LH

137
Q

closure of epiphyseal plates

A

testosterone indirectly closes the epiphyseal plates by converting to estrogen via aromatase

138
Q

Testosterone actions reproductive system before birth

A
  • Mediate differentiation of male genitalia, reproductive organs
  • Differentiation of Wolffian’s ducts and testicular descent
139
Q

Testosterone actions after birth

A

spermatogenesis, growth and maturation of reproductive system

140
Q

Testosterone actions non-reproductive actions

A

Anabolic action on muscles, bones (growth and narrow pelvic outlet), BMR
Heart, erythropoietin, fusion of the epiphyseal plate (indirect)

141
Q

Hypogonadism side effects

A

reduced steroidogenesis, spermatogenesis or both

142
Q

Hypergonadotropic hypogonadism

A

high FSH and LH bc of a problem in their receptors leading to no negative feedback

  • no response from gonads
  • Klinefelter’s
143
Q

Del Castillo syndrome

A

Sertoli cells but no spermatogonia cells

144
Q

Pampiniform countercurrent heat exchanger

A

Pampiniform plexus is cooler than blood coming down so it will cool entering blood

145
Q

AMH/MIF (anti-Müllerian hormone)

A

XY chromosomes then the embryonic testes will produce anti-Müllerian hormone. This causes the Müllerian (female) ducts to disappear
-secreted by sertoli cells

146
Q

Seminal vesicles

A
  • Supply fructose for energy
  • prostaglandins -> relax uterus/cervix, induce contraction
  • Secrete fibrinogen (thickens sperm to stay around cervix)
147
Q

Prostate gland

A
  • alkaline fluid that neutralizes vaginal acidity
  • clotting enzymes and fibrinolysin (liquefies sperm)
  • Provides PSA, and fibrin-degrading enzyme (dissolve cervical mucus)
  • prostasomes (adds Ca2+ channels to sperm)
148
Q

esophageal achalasia

A

Loss of LES inhibition

-closure of LES causing constant constriction of esophagus -> muscle deterioration

149
Q

antral pump

A

leading contraction closes pyloric sphincter, trailing contraction squeezes food against sphincter causing retropulsion decreasing particle size

  • gastin inc stimulation
  • ach inc contraction strength
  • NE and VIP dec contraction strength
150
Q

types of gastric reservoir relaxation

A

receptive: swallowing food
adaptive: distention of stomach
feedback: relax when nutrients in SI

151
Q

gastric emptying time

A

increase emptying: inc volume, isotonic

decrease: low pH, large particles, inc fat/caloric content

152
Q

migrating motor compelx

A

innervated by ENS
no MMC = bacteria growth
longer opening of depolarization gate = long reaching

153
Q

haustration

A

contracting and receiving segments hold on to their status for a significant amount of time -> ↑ water absorption

154
Q

interstitial cells of Cajal

A

pacemaker cells associated with the smooth musculature

activate circular fibers

155
Q

circular fibers vs longitudinal fibers

A

circular fibers: reduces the lumen diameter
-Pacemakers (Cajal) and excitatory musculomotor neurons activated
-Ca2+ via intracellular storage
longitudinal fibers: shortening the segment and expand the lumen
-Excitatory musculomotor neurons are main activators
-Ca2+ via influx

-both innervated by enteric nervous system (ENS)

156
Q

stomach and intestine vs. esophagus and gallbladder contraction

A
  • stomach and intestine contract spontaneously

- esophagus and gallbladder do not contract spontaneously

157
Q

Electomechanical coupling vs. Pharmacomechanical coupling

A
  • Electomechanical coupling: in skeletal and GI smooth muscles: Depolarization -> opening of voltage-gated Ca++ channels -> Ca++ influx of Ca++ -> contraction
  • Pharmacomechanical coupling: in smooth muscles only: Ligand activation of G-protein -> release of Ca++ from intracellular storages -> contraction without depolarization
158
Q

L-Channels

A

are responsible for the rapid inward current depolarization phase during gastric action potential (L-type Ca++ channel blockers -> disruption in GI motility)

159
Q

Sacral parasympathetics innervate the

A

distal half of the large intestine

160
Q

Efferent vagal fibers synapse with neurons of ENS in the

A

esophagus, stomach, small intestine, upper colon, gal bladder and pancreas

161
Q

paralytic ileus

A

no peristalsis in the GI tract

162
Q

Gastrocolic
Enterogastric
Colonoileal

Reflexes

A

Gastrocolic: eating -> bathroom
Enterogastric: chyme from stomach -> SI tells stomach to slow down
Colonoileal: distention of the colon -> ileum slow down

gut to PARAVERTEBRAL ganglia and back to the gut

163
Q

Reflexes from stomach and duodenum (vagovagal)
Pain reflexes
Defecation reflexes

A

Reflexes from stomach and duodenum (vagovagal)
Pain reflexes
Defecation reflexes

gut to spinal cord or brainstem and back to the gut

164
Q

Vagovagal reflex

A
  • Controls contraction in GI muscle layers in response to food stimuli
  • Efferents synapse with ENS to musculature are both inhibitory and stimulatory; efferents to secretory are ONLY excitatory
165
Q

Meyenteric plexus of Auerbach

A
  • motor, between longitudinal and circular layers

- Contains excitatory and inhibitory neurons

166
Q

Submucosal /Meissner plexus

A
  • Controls localized secretion and absorption

- absent in esophagus

167
Q

Afterhyperpolarization neurons

A
  • Long-lasting hyperpolarization potential
  • fulfill the role of interneurons
  • majority in myenteric plexus
168
Q

S-type neurons

A
  • All have nicotinic fast EPSPs

- Fast Na+ channels

169
Q

tetradoxin

A

Na+ channel blocker

170
Q

Excitatory secretomotor neurons release

A

ACh and VIP

171
Q

main excitatory neurotransmitters

A

ACh and substance P

172
Q

inhibitory neurotransmitters

A

ATP, VIP, nitric oxide and pituitary adenylate-cyclase

173
Q

Blood flow is directly related to local activity vasodilators

A

CCK, VIP, gastrin, secretin, kinins, NO, adenosine (metabolic byproduct of ATP consumption)

174
Q

shocks effect on villi

A

vasoconstriction of arteries bc of shock causes necrosis of villi resulting in decreases H2O absorption (loss of H2O)

175
Q

slow EPSP (AH-type and S-type)

A

Metabotropic receptors

  • AH-type cells is cAMP
  • S-type cells IP3 & Ca++ (PLC activation)
  • can be excite inhibitory/excitatory motor neurons resulting in prolonged contraction/secretion, contraction inhibition
176
Q

fast EPSP

A

Ionotropic receptors associated with a ion channel

-Most are mediated by ACh

177
Q

Slow inhibitory postsynaptic potentials (substance that activate)

A

Hyperpolarizing synaptic potential surpassing excitability

  • opioid peptide: constipation from opioids; diarrhea on naloxone treatment
  • NE (alpha2 receptor): S-type neurons -> reduce secretion
  • Galanin: slow IPSP in Auerbach’s plexus
  • Adenosine (A1 receptor): dec cAMP

Coffee antagonizes A1 receptors -> inc motility

178
Q

Presynaptic inhibition (mediators)

A

a neurotransmitter from one axon acts at receptors on 2nd axon to prevent the release of neurotransmitter from the 2nd axon

  • Serotonin suppresses fast and slow EPSPs in myenteric plexus
  • ACh negative feedback on self
  • Histamine: at H3 presynaptic receptors to suppress fast EPSPs in ENS
179
Q

Presynaptic facilitation

A
  • Enhances the neurotransmitter release and the amplitude of fast EPSPs at the myenteric plexus of small intestine and gastric antrum
  • NE inhibitory synapses at the submucosal plexus
  • Prokinetic drugs utilize this mechanism
180
Q

Metabotropic receptors bind slow EPSP

  • neurotransmitters
  • paracrine
  • hormone
A

neurotransmitters: serotonin, Ach, substance P
paracrine: histamine
hormone: gastrin, CCK

181
Q

Trisomies

A
  • Trisomy 21, 18, 13
  • Only full autosomal trisomies that can occur in nonmosaic form and lead to viable offspring mainly because the are among the most gene poor chromosomes
  • 21 > 18 > 13
182
Q

Down Syndrome types

A
  • Trisomy 21: Entire extra copy of 21st chromosome in each cell
  • Robertsonian translocation: Translocation between 21q and the long arm of the other acrocentric chromosomes
  • 21q21q translocation
  • Partial trisomy 21: Only part of the long arm of chromosome 21 is present in triplicate
183
Q

DiGeorge syndrome

A

deletion of segment of chromosome 22 resulting in craniofacial anomalies, intellectual disability, immunodeficiency and heart defects
-mediated by mishap in homologous recombination

184
Q

DiGeorge syndrome

A

deletion of segment of chromosome 22 resulting in craniofacial anomalies, intellectual disability, immunodeficiency and heart defects

  • mediated by mishap in homologous recombination
  • TBX1 plays role in heart defect
185
Q

Cri du chat syndrome

A

-Idiopathic Chromosomal Abnormality
-Hypertelorism (increased distance between eyes)
Epicanthus (skin fold of the upper eye lid)
Retrognathia (one jaw is set behind the other at longer distance than typical)
-larger deletion higher degree of intellectual disability

186
Q

sympathetic vs parasympathetic stimulation of salivary glands

A

para: stimulation -> ↑salivation directly and by ↑ blood flow
sympathetic: stimulation -> short-lived, smaller increase in saliva (through b adrenergic receptors), saliva is more viscous than with parasympathetic activation

187
Q

pyloric glands

A

Contain G cells (secrete gastrin) and mucous-secreting cells

188
Q

oxyntic (gastric) glands

A

Contain parietal cells (HCl & IF), endocrine cells, chief cells (pepsinogen) and mucous neck cells

189
Q

alkaline tide

A

from stomach

190
Q

Pepsinogen

A
  • secreted by chief cells
  • activated to pepsin at low pH
  • breaks down proteins to polypeptides
191
Q

Intrinsic factor

A

bind B12 and is absorbed in the distal ileum

192
Q

distal ileum direction will result in

A
  • pernicous anemia bc no B12 absorption

- trouble absorbing fat bc no recycling of bile

193
Q

acid tide

A

from pancreas

194
Q

Regulation of pancreatic secretion

A

Cephalic
Gastric
Intestinal

195
Q

Regulation of pancreatic secretion

A

Ach
secretin
CCK

196
Q

Brunner’s gland Inhibited by sympathetic tone important why?

A

When an individual has high stress sympathetic stimulation will inhibit Brunner’s gland resulting in no secretion of HCO3- and mucous -> ulcers

197
Q

primary bile acids and how they are formed

A

chenodeoxycholic acid
cholic acid

cyt P450

198
Q

Recycling mechanisms for bile salts

A

Diffusion
Carrier transport
Deconjugation, diffusion
Dehydroxylation

199
Q

AZF region

A

on Y chromosome and contain genes that appear to be important in spermatogenesis

200
Q

DAZ genes

A

deleted in azoospermia

201
Q

XY gonadal dysgenesis

A

SRY mutation
DAX1 duplication
SOX9 mutation
NR5A1 mutation

202
Q

Fragile X syndrome

A

FMR1 gene mutation (neural development disorder)

203
Q

Beckwith-Wiedemann Syndrome

A

Somatic overgrowth
Predisposition to childhood embryonal malignancies
Increased size of internal organs

Cause:
Loss of maternal ICR2/Kcnq1 methylation
Gain of H19 methylation
Paternal UPD for Igf2 cluster
11P15.5 duplication including Igf2
Point mutation in CDKN1C
204
Q

Silver-Russell syndrome

A

Growth retardation
Short stature

Cause:
Epimutation, loss of paternal ICR1 methylation

205
Q

IGF2

CDKN1C

A

IGF2: Over expression associated with cellular overgrowth
CDKN1C: Inhibitor of several G1 cyclin/cdk complexes

206
Q

Presynaptic inhibition mediators

A

CCK, ATP, histamine, NE and ACh

207
Q

Lower esophageal sphincter
Pyloric sphincter
Ileocolonic (ileocecal) sphincter
Internal anal sphincter

A 
Lower esophageal sphincter: incompetence -> heartburn and Barrett metaplasia
esophageal achalasia (failure of smooth muscles to relax

Pyloric sphincter: incompetence -> bile reflux -> gastritis and ulcers

Ileocolonic (ileocecal) sphincter: incompetence -> bacterial overgrowth in S.I. -> bloating and abdominal pain

Internal anal sphincter: incompetence  fecal incontinence

208
Q

Primary peristalsis vs Secondary peristalsis

A

Primary peristalsis: start of swallowing, the entire esophagus acts as a peristaltic receiving segment all the way down to the GE junction
Secondary peristalsis: Triggered by failure of the 1ry peristalsis to transport food to the stomach  stronger wave of propulsion

209
Q

regulator of gastric motility

A

ach: inc plateau
gastrin: stimulate pyloric pump
NE and VIP: dec plateau

210
Q

Receptive relaxation

A

Mechanoreceptors in pharynx during swallowing  afferent vagal  activation of efferent vagal  inhibitory musculomotor neurons in gastric ENS

211
Q

Adaptive relaxation

A

distension of gastric reservoir  vagovagal feed back  inhibitory musculomotor neurons in gastric ENS. (lost during diabetic neuropathy)

212
Q

Feedback relaxation

A

The presence of nutrients in SI  connections between receptors in SI and gastric ENS/or hormonal stimulation of the gastric ENS to gastric afferent vagal endings

213
Q

gastric emptying time factors

A 
Inc volume -> more rapid empyting
Larger particles -> slower
isotonic -> faster than hyper/hypo
more acidity -> slower
high fat (caloric count) -> slower
214
Q

chyme colon storage location

A

transverse colon

215
Q

dexamethasone

A

Synthetic glucocorticoids suppression of ACTH

216
Q

11BHSD1 vs 11BHSD2

A

11BHSD1: cortisone -> cortisol
11BHSD2: cortisol -> cortisone

217
Q

XIC

A

x inactivation center

218
Q

Cognitive skills

A

Ability to think, learn and solve problems. In babies (< 1 year), this looks like curiosity. This is how your child explores the world with their eyes, ears and hands. In toddlers (1-3 years), it also includes learning to count, naming colors and learning new words

219
Q

Social and emotional skills

A

Ability to relate to other people. Includes being able to express and control emotions. In babies, they smile at others and make sounds to communicate. In toddlers and preschoolers (3-5 years), they can ask for help, show and express feelings and get along with others.

220
Q

Speech and language skills

A

Ability to use and understand language. For babies, includes cooing and babbling. In older children, includes understanding what’s said and using words correctly that can be understood.

221
Q

Fine and gross motor skills

A

Ability to use small muscles (fine motor, particularly in the hands), and large muscles (gross motor). Babies use fine motor skills to grasp objects. Toddlers and preschoolers use them to hold utensils, work with objects and draw. Babies use gross motor skills to sit-up, roll-over and begin to walk. Older children use them to do things like jump, run and climb stairs.

222
Q

Activities of daily living

A

Ability to handle everyday tasks. For children, that includes eating, dressing and bathing themselves.

223
Q

Pancreatic a-amylase

A

hydrolyzes starch and glycogen -> maltose

224
Q

Disaccharidase deficiency

A

a

225
Q

FA humans can’t synthesize

A

omega 3/6

226
Q

pancreatic lipase

A

only breaks down triglycerides -> 2 FA and 2-monoglyceride

227
Q

Pancreatic colipase

A

(a peptide) binds to lipase and allows the lipase to the oil-water interphase, also counteracts the bile salt inhibition of lipase

228
Q

Phospholipase A2

A

is the major pancreatic enzyme for digesting PL -> lysophospholipids (e.g. lysolecithin) and FAs

229
Q

pancreatic cholesterol esterase

A

Cholesterol ester is hydrolyzed -> cholesterol and FA

230
Q

bile salts

A
  • Emulsification of fat droplets allows better digestion

- Emulsification of lipid (FA) digestion products allows better absorption

231
Q

Ezetimibe

A

Inhibit cholesterol importer causing no absorption of cholesterol

232
Q

acyl-CoA cholesterol acyltransferase

A

adds ester to cholesterol

233
Q

Poor fat absorption

A

deficiency in fat-soluble vitamins (A, D, E and K)

234
Q

Abetalipoproteinemia (no Apo B)

A

fats are absorbed into enterocyte but inability to make chylomicrons and VLDLs -> accumulation of lipid droplets in the cytoplasm of the enterocytes

TAG loading requires microsomal triglyceride transfer protein (MTP) to dock with ApoB-48 orApo-B100.

Deficiency of MPT -> abetalipoproteinemia

235
Q

Pepsin (endopeptidase)

A

proteins -> smaller polypeptides

236
Q

Pancreatic endopeptidases

A

Trypsin
Chymotrypsin
Elastase

237
Q

What can/not small intestine absorb

A

Di and tripeptides intestine can absorb but cant absorb disaccharides and triglycerides

238
Q

Pancreatic exopeptidase

A

Carboxypeptidase A

Carboxypeptidase B

239
Q

closure action in intestine

A

Colostrum rapidly diminishes the leakiness of the fetal intestine not allowing intact proteins to be absorbed

240
Q

Hartnup disease

Cystinuria

A

Hartnup disease: defective carrier for neutral AA (e.g. tryptophan)involves Cystinuria: carrier for basic AA (e.g. Lys, Arg) and the sulfur-containing AA (e.g. cystine)

241
Q

Vitamin A
where absorbed?
what happens with def.?

A

Retinol is the principle form

  • passively absorbed in the entire intestine by CHYLOMICRON
  • Vit A deficiency -> night blindness and skin lesions
242
Q

Vitamin D
where absorbed?
what happens with def.?

A
  • passively absorbed in the entire intestine by CHYLOMICRON

- Def. -> rickets / osteomalacia

243
Q

Vitamin E
where absorbed?
what happens with def.?

A
  • Transported in association with LIPOPORTEINS and RBCs

- Vit E deficiency -> fragile RBCs (antioxidant)

244
Q

Vitamin K
where absorbed?
what happens with def.?

A
  • Phyllaquinones is picked up by energy-dependent process in the PROXIMAL intestine and is incorporated into CHYLOMICRON
  • Def. -> excessive bleeding disorder (won’t have clotting factors
245
Q

What also can use NIS in the follicular cell?

What is pendrin used for?

A

NIS: Na+ I- symport
-bromide perchlorate thiocyanate

Cl- in exchange for I2

246
Q

RANKL and M-CSF

A

secretion from osteoblasts that increases osteoclast

247
Q

what is absorbed in the distal SI (ileum

A

B12, bile salts, and vitamin C

248
Q

vitamin C
where?
def?

A

ileum

scurvy

249
Q

vitamin B1
where?
def?

A

jejunum

beriberi

250
Q

vitamin B2
where?
def?

A

proximal small intestine

anorexia, impaired growth, nervous disorders

251
Q

niacin
where?
def?

A

all small intestine

Pellagra (dermatitis, dementia, and diarrhea) TRIPLE D

252
Q

vitamin B6
where?
def?

A

all small intestine

anemia, CNs disorder

253
Q

biotin
where?
def?

A

all small intestine

coenzyme for carboxylase enzymes -> def

254
Q

folic acid
where?
def?

A

facilitated transport

megablastic anemia, lesions, poor growth

255
Q

vitamin B12
where?
def?

A

B12 + intrinsic factor at distal ileum

pernicious anemia

256
Q

CCK effect

A

contraction of gallbladder
release digestive enzyme from pancreas
slow motility of stomach -> slower release of gastric contents into the small intestine

257
Q

jejunum vs ileum NaCl absorption

A

jejunum: Na+ in H+ out, Na+ in with aa or glucose
ileum: (Na+ in H+ out, HCO3- out Cl- in) Na+ and Cl- in

258
Q

BK channel activaiton

A
  • bacterial toxin inc adenyl cyclase -> inc BK channel

- upstream diarrhea causes shear stress on intestine -> inc BK channels

259
Q

Iron absorption (fast/slow)

A

Heme: fast
Non Heme: slow

Fe+ absorbed and bind/stored to apoferritin -> ferritin in enterocyte -> when to blood Fe+ passed to transferrin

260
Q

H2O absorption hypertonic vs hypotonic

A
  • hypertonic meal: water moves out to lumen first, then after the absorption of nutrients and electrolytes, water moves in (absorption in ileum and colon)
  • hypotonic meals starts immediately (primarily in jejunum and ileum)
261
Q

carnitine palmitoyltransferase-I

translocase

A

carnitine palmitoyltransferase-I: acyl CoA + carnitine = acyl-canitine

  • inhibited by malonyl CoA so not breaking down FA and building at same time
    translocase: transfers acyl-canitine across mitochondrial membrane
262
Q

ChREBP (carbohydrate response

element binding protein)

A

a TAG synthesis regulator that when high carbs will be activated to transcribe genes involved in making FA

  • long term
  • acetyl coa carboxylase long term
263
Q

secretin

A

in response to the low pH of the chyme entering the intestine causes the pancreas to release a solution rich in bicarbonate that helps neutralize the pH of the intestinal contents

264
Q

Serotonin

A

suppresses fast and slow EPSPs in myenteric plexus

265
Q

stimulation of parietal cells

A

gastrin, Ach, histamine

somatostatin and gastric inhibitory peptide inhibits

266
Q

VIP

A

inhibits muscular contraction

stimulates secretion -> increase diarrhea

267
Q

Prokinetic drugs

A

presynaptic facilitation -> increase the probability of gate opening -> enhance propulsion

268
Q

Bile acid-dependent and –independent bile canalicular flow

A

dependent: free bile exchanged for Na+ then conjugated to make bile salts

independent: Na+ exchanged for H+ leaving HCO3- in the cell to be added to bile
- + secretin

269
Q

estrogen

A

inhibits bile production

270
Q

scavenger-receptor B

A

receptor on liver that receives HDL

271
Q 
Apo A
Apo B (48)
Apo B (100)
Apo C
Apo E
A

Apo A: HDL -> LCAT
Apo B (48): chylomicron
Apo B (100): VLDL and LDL
Apo C: lipoprotein lipase (TAGs -> FA + glycerol)
Apo E: chylomicron binds to receptor on liver

272
Q

Carcinomas

A

arise from epithelial cells

  • Squamous cell carcinoma: protective epithelium
  • Adenocarcinoma: glandular epithelium
273
Q

Sarcomas

A

Sarcomas: begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue

274
Q

Hematopoeitic

A

Leukemia: malignancy of leukocytes
Lymphoma: tumors of B & T lymphocytes

275
Q

Neuroectodermal

A

arising from components of central and peripheral nervous system

276
Q

common alpha chain

A

FSH/LH and TSH

277
Q

Prolonged testosterone treatment

A

↓ GnRH receptors on gonadotrops

278
Q

low/high frequency GnRH release

A

Low-frequency: FSH release

high-frequency: LH release

279
Q

follistatin

A

produce by Sertoli cells with inhibin to deactivate activin

280
Q

prostaglandin during menstrual phase

A
  • vasoconstriction of endometrial vessels -> death

- myometrium contractions leading to the expulsion of blood and debris

281
Q

contraception

A

prevent ovulation by suppressing the LH surge

-thickening of cervical mucous

282
Q

Day after pill

A

progesterone antagonist preventing implantation by not allowing good development of endometrium

283
Q

Estrogens are bound to

Progesterone binds to

A
  • More estrogen bound to albumin but estrogen has a higher affinity for SHBG
  • increase in SHBG result in a high ratio of estrogen to androgens

-corticosteroid-binding protein

284
Q

Prostasome

A

linked to natural sperm activation

285
Q

fallopian tube

A

fimbrae -> infundibulum -> ampulla -> isthmus -> intramural

286
Q

Polyhydramnios

A

no closure of the esophagus due to higher than normal amniotic fluid

287
Q

is food digested?

is bile present?

A

before or after stomach

before of after bile duct in duodenum

288
Q

Annular pancreas

A

atresia or stenosis of duodenum because ventral and dorsal pancreatic buds encircle the duodenum

289
Q

Congenital omphalocel

A

mesenchymal defect where umbilical ring doesn’t close resulting in herniation of intestines
-similar to Gastroschisis

290
Q

midgut non rotation

A
  • small intestines sitting on the right side and large intestine on the left side
  • volvulus can cause occlusion of SMA -> intestinal ischemia
291
Q

mixed rotation and volvulus

A
  • cecum just below pylorus, fixed to post wall

- can cause duodenal obstruction

292
Q

reversed rotation

A

SMA obstructs the transverse colon and can also cause reduced blood flow through SMA

293
Q

Subhepatic cecum and appendix

A

cecum stuck to the inf surface of the liver resulting in the appendix being located in the upper right quadrant

294
Q

internal hernia

A

intestinal loop passes through mesenteric defect, can cause strangulation/obstruction

295
Q

midgut volvulus

A

large intestine twist over the duodenum

296
Q

Omphaloenteric duct remnants

A

ductal remnants develop into cyst in the umbilicus or just below

  • can have persistent vitelline artery
  • sirenomelia
297
Q

Ileal diverticulum

A

small out pouching of the ileum with a remnant of vitelline duct
-dark feces from upper GI bleeding

298
Q

Hirschsprung disease

A
  • aka congenital megacolon
  • Neural crest cells don’t migrate properly during weeks 5-7 and the myenteric plexus doesn’t have autonomic ganglion cells
299
Q

persistent cloaca

A

common outlet of intestinal, urinary, and reproductive tract

300
Q

anorectal agenesis with rectovaginal fistula

A

rectum opens up into vagina

301
Q

lesser omentum and falciform ligament are derived from

A

ventral mesentery

302
Q

Primary retroperitoneals

A 
Kidneys
Adrenal glands
Aorta
IVC
Caudal rectum
Anal canal
303
Q

Forgot includes and blood supply

A

stomach, Duodenum to just distal to the bile duct opening, liver, biliary apparatus

celiac trunk

304
Q

omphaloenteric duct is obliterated by this point

A

week 11

305
Q

midgut includes and blood supply

A

distal half of the duodenum, jejunum, ileum, cecum, ascending colon, and the proximal half transverse colon

SMA

306
Q

hindgut

A

½ of the transverse colon, the descending colon, sigmoid colon, rectum, and anal canal cranial to the pectinate line

IMA

307
Q

painful vs non-painful Bright red vs dark blood from hemorrhoids

A

Internal hemorrhoids - no pain, dark blood

External hemorrhoids - painful, bright red blood

308
Q

HMG CoA reductase

A

rate limiting enzyme for cholesterol synthesis

309
Q

SREBP

A

binds when low cholesterol to inc enzymes needed for cholesterol synthesis

310
Q

Estradiol (E2) effects

A
  • inhibit osteoclast -> osteoporosis
  • inc metabolism -> fatigue
  • Na+ and H2O retention
  • vaginal cornification -> painful intercourse bc thin vaginal wall
  • thin mucous (ferning)
  • inc progesterone receptors
311
Q

gastrin effect on bile

A
  • directly inc bile in liver

- indirect inc by dec pH causing release of secretin (secretin inc HCO3- production in bile)

312
Q

lithocolic acid

A

secondary bile acid that cannot be absorbed

313
Q

alc effect on acetaminophen metabolism

A

inc P450 pathway diverting from GSH pathway

-inc in NAPQ1

314
Q

zone I

zone III

A

zone I: glycogen and plasma protein synthesis

zone III: detox

315
Q

MALE
mesospheric duct
urogenital sinus

A

mesospheric duct: epididymis, ductus deferens, seminal gland, efferent ductules
urogenital sinus: bladder, spongy urethra, bulbourethra, prostate (also mesenchyme)

316
Q

FEMALE
paramesospheric duct
urogenital sinus

A

paramesospheric duct: uterus, uterine tubes

urogenital sinus: urethra, paraurethra, greater vestibular gland

317
Q 
Hepatocyte
RER
SER
Gogli
peroxisomes
A

RER: synthesis of plasma proteins
SER: biotransformatio/detox
Gogli: plasma protein and bile components
peroxisomes: oxidize FA

318
Q

Dark granules

Light Granules

A

Dark granules: NE

Light Granules: Epi

319
Q

Liver deterioration

A

fatty liver -> steatohepatitis -> cirrhosis -> liver failure

320
Q

Barrett’s esophagus

A

stratified squamous -> simple columnar

321
Q

Transitional zone

Peripheral zone

A

Transitional zone: benign hyperplasia

Peripheral zone: adenocarcinoma

322
Q

OPG

A

osteoclast inhibiitor

323
Q

Parotid
submandibular
sublingual

A

Parotid: serous acini cells

submandibular: serous acini cells and mucosal acini cells
sublingual: mucosal acini cells

324
Q

Dentin
Enamel
Cementum

A

Dentin: odontoblast
Enamel: ameloblast
Cementum: cementoblast, anchors periodontal ligament to roots of tooth

BECOM 2 (7 decks)

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