BECOM Exam #4 Flashcards
Pituitary part names
Ant: pars distalis Post: pars nervosa pas intermedia (in between ant and post) infundibular stalk pars tubulars (surrounds infundibular stalk)
Posterior innervation and secretion (from hypothalamus)
paraventricular nucleus: oxytocin
supraoptic nucleus: ADH
Anterior communication with hypothalamus
hypophyseal portal vein
Hypophyseal pouch ectoderm forms
ant pituitary
Neurohpoyseal pouch neuroectoderm forms
post pituitary
anterior pituitary cells and function (acidophils and basophils)
- Acidophils – contain polypeptide hormones
- Somatotrophs – secrete growth hormone (GH, aka somatotropin)
- Mammotrophs (aka Lactotrophs) – secrete prolactin (PRL)
- Basophils – contain glycoprotein hormones
- Gonadotrophs – secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH)
- Thyrotrophs – secrete thyrotropin (TSH)
- Corticotrophs – secrete adrenal corticotropin (ACTH) and lipotropin (LPH)
Pars intermedia cell type
corticotrophs
chromotrophs
Pars Tubularis cell type
gonadotrophs
Pituitary adenomas types (cell types and hormone)
gigantism
loss of mensural cycle
Cushing disease
gigantism: somatotrohs -> GH
loss of mensural cycle: lactotrophs -> prolactin
Cushing disease: thyrotrophs -> hyperthyroidism
Thyroid cell type and hormone
Follicular cell (thyocyte): thyroglobulin Parafollicular cells (c cells): calcitonin
parathyroid cell type and hormone
principal cells: parathyroid hormone (PTH)
oxyphil cells: some PTH but mainly nonfunctional
Adrenal Cortex layers and steroids
- capsule
- zona glomerulosa: mineralcoticoids (aldosterone)
- zona fasciculata: glucocorticoids (cortisol)
- zona recticularis: dehydroepiandrosterone DHEA a precursor to testosterone
- adrenal medulla: epinephrine and norepinephrine
Addison’s disease
destruction of particular cell type of adrenal cortex
-KNOW layers and correlate to different symptoms of Addison’s disease
Pineal Gland contents and release
corpus arenaceum (brain) sand: releases melatonin
POMC
POMC is cleaved into
- ACTH and B-lipoprotein (B-LPS)
- ACTH contain alpha-MSH
Pregnancy can cause infarction in the pituitary
d
Serous inflammation
Excess watery fluid exudate…blisters
Serofibrinous inflammation
Exudate rich in fibrin
Catarrhal inflammation
Mild inflammation of mucous membrane with excess watery secretion
acid fast pos. gastrointestinal protozoa
Cryptosporidia, Cyclospora
Giardiasis
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)
Cryptosporidium
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
Cyclospora
Similar manifestations as cryptosporidium but larger histologically
-ACID-FAST positive
Amebiasis
Causative agent: Entamoeba histolytica
Manisfestations: amoebic dysentery (traveler’s dysentery)
-histologically will contain RBCs within
toxoplasma gondii
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
Acanthamoeba
- effects eye usually through effected contacts
- found in USA
Naegleria fowleri
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
trypansoma brucii
Disease: African Sleeping Sickness Manifestation: characterized mainly by sleeping problems insomnia or sleepiness Transmission: Tsetse fly (painful bite) Diagnosis: Trypomastigote in blood smear -AFRICA
plasmodium
P. falciparum
P. malariae (Anopheles mosquitoes)
P. vivax
P. ovale
plasmodium falciparum
Manifestation: cerebral hemorrhaging and blood in urine (lyses 10% of blood cells)
Diagnosis: produces banana shaped
babesiosis
Manifestation: fever and hemolytic anemia:
Transmission: US tickborne illness
Diagnosis: Maltese Cross on histological slide
Trichomonas vaginalis
Manifestation: foul-smelling greenish discharge
Transmission: sexual
Diagnosis: Motile ‘pear-shaped’ trophozoites and strawberry cervix
leishanosma spp
Disease: Visceral leishmaniasis (fatal) or Cutaneous leishmaniasis
Transmission: Sandfly
Diagnosis: Macrophages with amastigotes
trypanosma cruzi
Disease: cardiomegaly, megacolon, and megaesophagus (Chagas Disease) or unilateral periorbital swelling
Transmission: kissing bug
Diagnosis: Trypomastigote in blood smear
mites vs lice
mites, scabies, and chiggers: burrow
lice: don’t jump, close contact
17alpha hydroxylase def
- 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
21 hydroxylase (CYP21A2) def
- normal levels of DHEA and aldosterone but low cortisol levels
- KEY LOW 11-deoxycortisol
11 B hydroxylase (CYP11B1) def
- normal levels of DHEA and aldosterone but low cortisol levels
- KEY HIGH 11-deoxycortisol
aldosterone vs cortisol binding to albumin and CBG
cortisol has a higher affinity for CBG than aldosterone
-inc cortisol will unbind aldosterone from CBG increasing blood aldosterone levels
Side effects of aldosterone excess
- 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
Aldosterone escape
Aldosterone increase -> increase in Na+ retention -> transient increase in arterial BP -> pressure diuresis and increased ANP secretion (natriuresis)
Cortisol metabolic functions
- 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
Cushing Disease
- 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
Tg time in the follicle
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
T3 vs T4
T3: active
T4: inactive
DIT and MIT
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
Selenodeionidases (D1 vs D2 vs D3)
D1: T4 -> T3 (liver, kidneys and thyroid tissue)
D2: T4 -> T3 (CNS)
D3: inactivates T3 to DIT and T4 to RT3
Goiter syndrome
-is an enlargement of the thyroid gland in the neck
Causes:
-low iodine -> low T3 -> no negative feedback
-
T3 function
- 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
T3 and T4 function (nuclear)
-Nuclear activation and non classical activation of membrane receptor (both T3 and T4) -> synthesis of new proteins
Giant Cell
multinucleated cells that form as a result of Granulomatous Inflammation
Caseating granuloma vs Noncaseating granulomas
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
vitamin D activation
Cholecalciferol -> 25-hydroxycholecalciferol –(PTH)–> 1,25-dihydroxycholecaliferol
high calcium or low PTH decrease 25-hydroxycholecalciferol -> 1,25-dihydroxycholecaliferol
Vitamin D actions
↑ intestinal calbindin ↑Ca++ absorption
↑ Ca++-dependent ATPase and alkaline phosphatase
↑ phosphate flux through the intestinal epithelium
↑ Ca++ and phosphate renal secretion (minimal effect)
b cells:
a cells:
d cells:
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
GLP-1, GIP and CCK (incretins)
- primes the b cells for the incoming hyperglycemia
- GLP-1 surpasses glucagon
- Dipeptidyl peptidase IV inhibitors increase GLP-1 and improve glucose tolerance
tyrosine-phosphatases (PTP)
terminates insulin receptor signaling
- ex. PTP1B and leucocyte antigen-related (LAR) phosphatase
- over expression in patients with insulin resistant diabetes
stress affect on ACTH
- 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
Diurnal variation and ACTH
- 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
Metabolic (direct) actions of GH
- 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
Anabolic actions of GH
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
IGF-1
- bone growth
- muscle growth (inc AA uptake and inc protein synth)
- cartilage growth
Gigantism
high GH before epiphyseal closure
Acromegaly
high GH after epiphyseal closure -> disproportionate growth
Symptoms and signs of GH excess
- 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
High ADH (SIADHS)
- Hyponatremia (increase volume -> release ANP -> secrete Na+)
- Concentrated urine
- Elevated urinary Na
StAR
after cholesterol ester is cleaved by cholesterol esterase StAR is used to transport cholesterol across the mitochondrial membrane so steroidogenesis can occur
Zona glomerulosa
- lacks CYP17A1 (17a-hydroxylase) and cannot produce DHEA or glucocorticoids
- aldosterone production
Primary hyperaldosteronism vs Secondary hyperaldosteronism
Primary hyperaldosteronism: adrenal tumor
Secondary hyperaldosteronism: high activity of the renin-angiotensin system
pregnancy effect on CBG
increase CBG which will increase total T3/T4 but normal T3/T4 blood levels
In long term cortisol excess
- increased adipocytes differentiation (centripetal obesity)
- increase cortisol neg feedback threshold
oxytocin during development
cardiomyocytes and neural development
cortisol during development
Lung maturation
Dehydroepiandrosterone (DHEA)
-Responsible for adrenarche (early stage sexual maturation) before or around puberty in male and female
Dehydroepiandrosterone (DHEA) during pregnancy
In placenta, 16a-OH-DHEA is converted to 16a-OH-androstenedione and then to estriol (E3)
Adrenogenital syndrome
adult females
newborn females
prepubertal males
adult females: deep voice, large muscles, fascial hair, breast become smaller
newborn females: partially male-type external genitalia
prepubertal males: Precocious pseudopuberty
TPO activity is stimulated by
Stimulated
- TSH (which also increases NIS, follicular cell proliferation and Tg endocytosis)
- hCG of pregnancy
hCG
mimics TSH on follicular thyroid cells
T3 during development
neonatal brain development
Metabolic actions of thyroid hormones
↑Glucose absorption from the intestine
↑Glycolysis, gluconeogenesis and oxidative phosphorylation
↑Lipolysis, ↑ LDL ↓ plasma cholesterol
↑Protein synthesis and degradation (net effect is catabolic)
Thyroid actions on cardiovascular system
- 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
JAK/STAT
GH and prolactin
somatomedin C
IGF-I
longer half-life than GH
PC1/3
clips out of the c peptide (proinsulin -> insulin) and cleaves POMC????????????
PTH-related peptide
can be released by tumors and have nothing to do with the parathyroid causing hypercalemia
low dose Vitamin D vs high dose
Small quantities -> promotes bone calcification
Extreme dose of Vit D -> bone resorption
paid PTH effect
slow PTH effect
other effect:
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
excessive Ca2+
decrease parathyroid size
-High Ca++ -> stimulation of Ca++ sensing receptor/CaSR (G-coupled protein) -> activation of IP3, DAG and intracellular Ca++ -> ↓ PTH secretion
Calcitonin
- 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
PTH hypersecretion
- hypercalcemia (causes hyporeflexia and muscle weakness)
- hyperphosphaturia (bc osteoclast inc alkaline phosphatase)
- renal stones
- bone decalcification
PTH hyposecretion
-hypocalcemia (causes hyperreflexia and tetany)
-hyperphosphatemia
-
Vitamin D deficiency
soft bones (rickets and osteomalacia) bc getting Ca2+ from bones
amylin
- reduces gastric emptying (satiety)
- inhibits glucagon
somatostatin
- inhibits secretion of insulin, glucagon, and pancreatic peptide
- stimulate glucose and amino acid ingestion
- reduce GI motility
sulfonylurea
blocks K+ channel on pancreatic B cells causing depolarization and insulin release
finsulin promotes
- glycogen synthesis
- glycolysis
- lipogenesis (dec ketone bodies)
- protein synthesis
- Increases GLUT4 expression
moderate exercise vs. intense exercise vs. stress
- 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
glucagon stimulated by and increases
Hypoglycemia
Increased amino acids
Norepinephrine
Epinephrine
↑ hepatic glycogenolysis
Gluconeogenesis
Lipolysis
how does oxytocin cause contraction
PLC and PKC cause inc Ca2+ -> contraction
Leydig cell function
release testosterone into blood vessels and seminiferous tubules
Sertoli cell function
- 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)
Cryptorchidism
when the testis don’t descend and temp is 37-38 which won’t allow spermatogenesis to occur
Spermatogonial Phase
Type A dark: resident processor cell
Type A pale: divide into type B cell
Type B: differentiate into spermatocyte
Spermatocyte Phase
Primary spermatocyte: meiosis I, large cell
Secondary spermatocyte: meiosis II, smaller cell
Spermiogenesis Phase
- 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
Chemical Mediators (PAMPs and corresponding receptors)
Endotoxin TLR4 Lipoproteins TLR1, 2, 6 Peptidoglycan NOD 1 & 2 Heat shock proteins TLR2 and 4 Bacterial DNA TLR9 Bacterial RNA TLR3, TLR7, TLR8
Chemical Mediators (DAMPS and corresponding receptors)
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
Extravation
- 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
IL-1B, IL-6, TNF-a
cytokines that signal for acute phase proteins (mainly IL-6), neutrophil mobilization, increase body temp
acute phase proteins and purpose
C-reactive protein (opsonization)
mannose-binding lectin
fibrinogen (clotting factor)
Chemokines attract what cell CXCL8 CXCL7 CCL3 CCL5 CXCL-1
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
Transudate edema
extravascular fluid with low protein content
-due to increase hydrostatic pressure
Exudate edema
mast of cells and fluid seeping out of blood vessels
-due to increase vascular permeability
Suppurative (Purulent) vs Non-Suppurative
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
mesonephric duct forms
f
Amoebic vs Bacterial Dysentery
Amoebic: Entamoeba histolytica
-variable fever
Bacterial: Shigella spp
-high fever
BOTH will have fecal leukocytes
Classical vs. Alternative Macrophage actions
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
Importance of LH surge
- 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
NSAIDs effect on menstrual period?
cause heavier bleeding bc blood is thinner and prostaglandin is inhibited causing no uterine contractions (help expel blood and debri)
fibrinolysin
prevent menstrual blood from coagulating
-Heavy menstrual cycle will have clots bc little fibrinolysin
collegenase
high during LH surge allowing ovulation of egg
cervical mucous (estrogen and progesterone)
- 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
Menopause
- 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
high androgens and infertility
- 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
Female reproductive tract aids in sperm migration
- 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
Zona reaction
Release of cortical oocyte granules causes oocyte membrane to become impenetrable to other sperm
Progesterone functions after fertilization
- 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)
respiration rate during pregnancy and result
Icn bicarb in pregnant women urine bc inc CO2 exhalation causing respiratory alkalosis, kidney will secrete bicarb in response
Human Chorionic gonadotropin (hCG) (placenta hormone)
- 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
Human chorionic somatomammotropin (placenta hormone)
- 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
Estrogen (Estriol/E3) (placenta hormone)
- 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)
Progesterone (placenta hormone)
- 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
Insulin (fetal hormone)
- Increased in response to excess maternal glucose
- In uncontrolled diabetic mothers, increased insulin has anabolic effects on the fetus -> oversized newborn
androgen in regulating GnRH pulsatility
- inhibition of GnRH pulse frequency is antagonized by androgens
- dec LH and FSH
- Testosterone has a direct inhibition effect on GnRH
stress effect on GnRH
CRH, ADH, ACTH, endogenous opioid peptides (e.g., β-endorphin), and cortisol surpasses GnRH
what determines the half life of a hormone
amount of glycosylation
-FSH has longer half-life in circulation than LH
closure of epiphyseal plates
testosterone indirectly closes the epiphyseal plates by converting to estrogen via aromatase
Testosterone actions reproductive system before birth
- Mediate differentiation of male genitalia, reproductive organs
- Differentiation of Wolffian’s ducts and testicular descent
Testosterone actions after birth
spermatogenesis, growth and maturation of reproductive system
Testosterone actions non-reproductive actions
Anabolic action on muscles, bones (growth and narrow pelvic outlet), BMR
Heart, erythropoietin, fusion of the epiphyseal plate (indirect)
Hypogonadism side effects
reduced steroidogenesis, spermatogenesis or both
Hypergonadotropic hypogonadism
high FSH and LH bc of a problem in their receptors leading to no negative feedback
- no response from gonads
- Klinefelter’s
Del Castillo syndrome
Sertoli cells but no spermatogonia cells
Pampiniform countercurrent heat exchanger
Pampiniform plexus is cooler than blood coming down so it will cool entering blood
AMH/MIF (anti-Müllerian hormone)
XY chromosomes then the embryonic testes will produce anti-Müllerian hormone. This causes the Müllerian (female) ducts to disappear
-secreted by sertoli cells
Seminal vesicles
- Supply fructose for energy
- prostaglandins -> relax uterus/cervix, induce contraction
- Secrete fibrinogen (thickens sperm to stay around cervix)
Prostate gland
- 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)
esophageal achalasia
Loss of LES inhibition
-closure of LES causing constant constriction of esophagus -> muscle deterioration
antral pump
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
types of gastric reservoir relaxation
receptive: swallowing food
adaptive: distention of stomach
feedback: relax when nutrients in SI
gastric emptying time
increase emptying: inc volume, isotonic
decrease: low pH, large particles, inc fat/caloric content
migrating motor compelx
innervated by ENS
no MMC = bacteria growth
longer opening of depolarization gate = long reaching
haustration
contracting and receiving segments hold on to their status for a significant amount of time -> ↑ water absorption
interstitial cells of Cajal
pacemaker cells associated with the smooth musculature
activate circular fibers
circular fibers vs longitudinal fibers
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)
stomach and intestine vs. esophagus and gallbladder contraction
- stomach and intestine contract spontaneously
- esophagus and gallbladder do not contract spontaneously
Electomechanical coupling vs. Pharmacomechanical coupling
- 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
L-Channels
are responsible for the rapid inward current depolarization phase during gastric action potential (L-type Ca++ channel blockers -> disruption in GI motility)
Sacral parasympathetics innervate the
distal half of the large intestine
Efferent vagal fibers synapse with neurons of ENS in the
esophagus, stomach, small intestine, upper colon, gal bladder and pancreas
paralytic ileus
no peristalsis in the GI tract
Gastrocolic
Enterogastric
Colonoileal
Reflexes
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
Reflexes from stomach and duodenum (vagovagal)
Pain reflexes
Defecation reflexes
Reflexes from stomach and duodenum (vagovagal)
Pain reflexes
Defecation reflexes
gut to spinal cord or brainstem and back to the gut
Vagovagal reflex
- 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
Meyenteric plexus of Auerbach
- motor, between longitudinal and circular layers
- Contains excitatory and inhibitory neurons
Submucosal /Meissner plexus
- Controls localized secretion and absorption
- absent in esophagus
Afterhyperpolarization neurons
- Long-lasting hyperpolarization potential
- fulfill the role of interneurons
- majority in myenteric plexus
S-type neurons
- All have nicotinic fast EPSPs
- Fast Na+ channels
tetradoxin
Na+ channel blocker
Excitatory secretomotor neurons release
ACh and VIP
main excitatory neurotransmitters
ACh and substance P
inhibitory neurotransmitters
ATP, VIP, nitric oxide and pituitary adenylate-cyclase
Blood flow is directly related to local activity vasodilators
CCK, VIP, gastrin, secretin, kinins, NO, adenosine (metabolic byproduct of ATP consumption)
shocks effect on villi
vasoconstriction of arteries bc of shock causes necrosis of villi resulting in decreases H2O absorption (loss of H2O)
slow EPSP (AH-type and S-type)
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
fast EPSP
Ionotropic receptors associated with a ion channel
-Most are mediated by ACh
Slow inhibitory postsynaptic potentials (substance that activate)
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
Presynaptic inhibition (mediators)
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
Presynaptic facilitation
- 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
Metabotropic receptors bind slow EPSP
- neurotransmitters
- paracrine
- hormone
neurotransmitters: serotonin, Ach, substance P
paracrine: histamine
hormone: gastrin, CCK
Trisomies
- 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
Down Syndrome types
- 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
DiGeorge syndrome
deletion of segment of chromosome 22 resulting in craniofacial anomalies, intellectual disability, immunodeficiency and heart defects
-mediated by mishap in homologous recombination
DiGeorge syndrome
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
Cri du chat syndrome
-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
sympathetic vs parasympathetic stimulation of salivary glands
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
pyloric glands
Contain G cells (secrete gastrin) and mucous-secreting cells
oxyntic (gastric) glands
Contain parietal cells (HCl & IF), endocrine cells, chief cells (pepsinogen) and mucous neck cells
alkaline tide
from stomach
Pepsinogen
- secreted by chief cells
- activated to pepsin at low pH
- breaks down proteins to polypeptides
Intrinsic factor
bind B12 and is absorbed in the distal ileum
distal ileum direction will result in
- pernicous anemia bc no B12 absorption
- trouble absorbing fat bc no recycling of bile
acid tide
from pancreas
Regulation of pancreatic secretion
Cephalic
Gastric
Intestinal
Regulation of pancreatic secretion
Ach
secretin
CCK
Brunner’s gland Inhibited by sympathetic tone important why?
When an individual has high stress sympathetic stimulation will inhibit Brunner’s gland resulting in no secretion of HCO3- and mucous -> ulcers
primary bile acids and how they are formed
chenodeoxycholic acid
cholic acid
cyt P450
Recycling mechanisms for bile salts
Diffusion
Carrier transport
Deconjugation, diffusion
Dehydroxylation
AZF region
on Y chromosome and contain genes that appear to be important in spermatogenesis
DAZ genes
deleted in azoospermia
XY gonadal dysgenesis
SRY mutation
DAX1 duplication
SOX9 mutation
NR5A1 mutation
Fragile X syndrome
FMR1 gene mutation (neural development disorder)
Beckwith-Wiedemann Syndrome
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
Silver-Russell syndrome
Growth retardation
Short stature
Cause:
Epimutation, loss of paternal ICR1 methylation
IGF2
CDKN1C
IGF2: Over expression associated with cellular overgrowth
CDKN1C: Inhibitor of several G1 cyclin/cdk complexes
Presynaptic inhibition mediators
CCK, ATP, histamine, NE and ACh
Lower esophageal sphincter
Pyloric sphincter
Ileocolonic (ileocecal) sphincter
Internal anal sphincter
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
Primary peristalsis vs Secondary peristalsis
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
regulator of gastric motility
ach: inc plateau
gastrin: stimulate pyloric pump
NE and VIP: dec plateau
Receptive relaxation
Mechanoreceptors in pharynx during swallowing afferent vagal activation of efferent vagal inhibitory musculomotor neurons in gastric ENS
Adaptive relaxation
distension of gastric reservoir vagovagal feed back inhibitory musculomotor neurons in gastric ENS. (lost during diabetic neuropathy)
Feedback relaxation
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
gastric emptying time factors
Inc volume -> more rapid empyting Larger particles -> slower isotonic -> faster than hyper/hypo more acidity -> slower high fat (caloric count) -> slower
chyme colon storage location
transverse colon
dexamethasone
Synthetic glucocorticoids suppression of ACTH
11BHSD1 vs 11BHSD2
11BHSD1: cortisone -> cortisol
11BHSD2: cortisol -> cortisone
XIC
x inactivation center
Cognitive skills
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
Social and emotional skills
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.
Speech and language skills
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.
Fine and gross motor skills
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.
Activities of daily living
Ability to handle everyday tasks. For children, that includes eating, dressing and bathing themselves.
Pancreatic a-amylase
hydrolyzes starch and glycogen -> maltose
Disaccharidase deficiency
a
FA humans can’t synthesize
omega 3/6
pancreatic lipase
only breaks down triglycerides -> 2 FA and 2-monoglyceride
Pancreatic colipase
(a peptide) binds to lipase and allows the lipase to the oil-water interphase, also counteracts the bile salt inhibition of lipase
Phospholipase A2
is the major pancreatic enzyme for digesting PL -> lysophospholipids (e.g. lysolecithin) and FAs
pancreatic cholesterol esterase
Cholesterol ester is hydrolyzed -> cholesterol and FA
bile salts
- Emulsification of fat droplets allows better digestion
- Emulsification of lipid (FA) digestion products allows better absorption
Ezetimibe
Inhibit cholesterol importer causing no absorption of cholesterol
acyl-CoA cholesterol acyltransferase
adds ester to cholesterol
Poor fat absorption
deficiency in fat-soluble vitamins (A, D, E and K)
Abetalipoproteinemia (no Apo B)
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
Pepsin (endopeptidase)
proteins -> smaller polypeptides
Pancreatic endopeptidases
Trypsin
Chymotrypsin
Elastase
What can/not small intestine absorb
Di and tripeptides intestine can absorb but cant absorb disaccharides and triglycerides
Pancreatic exopeptidase
Carboxypeptidase A
Carboxypeptidase B
closure action in intestine
Colostrum rapidly diminishes the leakiness of the fetal intestine not allowing intact proteins to be absorbed
Hartnup disease
Cystinuria
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)
Vitamin A
where absorbed?
what happens with def.?
Retinol is the principle form
- passively absorbed in the entire intestine by CHYLOMICRON
- Vit A deficiency -> night blindness and skin lesions
Vitamin D
where absorbed?
what happens with def.?
- passively absorbed in the entire intestine by CHYLOMICRON
- Def. -> rickets / osteomalacia
Vitamin E
where absorbed?
what happens with def.?
- Transported in association with LIPOPORTEINS and RBCs
- Vit E deficiency -> fragile RBCs (antioxidant)
Vitamin K
where absorbed?
what happens with def.?
- 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
What also can use NIS in the follicular cell?
What is pendrin used for?
NIS: Na+ I- symport
-bromide perchlorate thiocyanate
Cl- in exchange for I2
RANKL and M-CSF
secretion from osteoblasts that increases osteoclast
what is absorbed in the distal SI (ileum
B12, bile salts, and vitamin C
vitamin C
where?
def?
ileum
scurvy
vitamin B1
where?
def?
jejunum
beriberi
vitamin B2
where?
def?
proximal small intestine
anorexia, impaired growth, nervous disorders
niacin
where?
def?
all small intestine
Pellagra (dermatitis, dementia, and diarrhea) TRIPLE D
vitamin B6
where?
def?
all small intestine
anemia, CNs disorder
biotin
where?
def?
all small intestine
coenzyme for carboxylase enzymes -> def
folic acid
where?
def?
facilitated transport
megablastic anemia, lesions, poor growth
vitamin B12
where?
def?
B12 + intrinsic factor at distal ileum
pernicious anemia
CCK effect
contraction of gallbladder
release digestive enzyme from pancreas
slow motility of stomach -> slower release of gastric contents into the small intestine
jejunum vs ileum NaCl absorption
jejunum: Na+ in H+ out, Na+ in with aa or glucose
ileum: (Na+ in H+ out, HCO3- out Cl- in) Na+ and Cl- in
BK channel activaiton
- bacterial toxin inc adenyl cyclase -> inc BK channel
- upstream diarrhea causes shear stress on intestine -> inc BK channels
Iron absorption (fast/slow)
Heme: fast
Non Heme: slow
Fe+ absorbed and bind/stored to apoferritin -> ferritin in enterocyte -> when to blood Fe+ passed to transferrin
H2O absorption hypertonic vs hypotonic
- 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)
carnitine palmitoyltransferase-I
translocase
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
ChREBP (carbohydrate response
element binding protein)
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
secretin
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
Serotonin
suppresses fast and slow EPSPs in myenteric plexus
stimulation of parietal cells
gastrin, Ach, histamine
somatostatin and gastric inhibitory peptide inhibits
VIP
inhibits muscular contraction
stimulates secretion -> increase diarrhea
Prokinetic drugs
presynaptic facilitation -> increase the probability of gate opening -> enhance propulsion
Bile acid-dependent and –independent bile canalicular flow
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
estrogen
inhibits bile production
scavenger-receptor B
receptor on liver that receives HDL
Apo A Apo B (48) Apo B (100) Apo C Apo E
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
Carcinomas
arise from epithelial cells
- Squamous cell carcinoma: protective epithelium
- Adenocarcinoma: glandular epithelium
Sarcomas
Sarcomas: begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue
Hematopoeitic
Leukemia: malignancy of leukocytes
Lymphoma: tumors of B & T lymphocytes
Neuroectodermal
arising from components of central and peripheral nervous system
common alpha chain
FSH/LH and TSH
Prolonged testosterone treatment
↓ GnRH receptors on gonadotrops
low/high frequency GnRH release
Low-frequency: FSH release
high-frequency: LH release
follistatin
produce by Sertoli cells with inhibin to deactivate activin
prostaglandin during menstrual phase
- vasoconstriction of endometrial vessels -> death
- myometrium contractions leading to the expulsion of blood and debris
contraception
prevent ovulation by suppressing the LH surge
-thickening of cervical mucous
Day after pill
progesterone antagonist preventing implantation by not allowing good development of endometrium
Estrogens are bound to
Progesterone binds to
- 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
Prostasome
linked to natural sperm activation
fallopian tube
fimbrae -> infundibulum -> ampulla -> isthmus -> intramural
Polyhydramnios
no closure of the esophagus due to higher than normal amniotic fluid
is food digested?
is bile present?
before or after stomach
before of after bile duct in duodenum
Annular pancreas
atresia or stenosis of duodenum because ventral and dorsal pancreatic buds encircle the duodenum
Congenital omphalocel
mesenchymal defect where umbilical ring doesn’t close resulting in herniation of intestines
-similar to Gastroschisis
midgut non rotation
- small intestines sitting on the right side and large intestine on the left side
- volvulus can cause occlusion of SMA -> intestinal ischemia
mixed rotation and volvulus
- cecum just below pylorus, fixed to post wall
- can cause duodenal obstruction
reversed rotation
SMA obstructs the transverse colon and can also cause reduced blood flow through SMA
Subhepatic cecum and appendix
cecum stuck to the inf surface of the liver resulting in the appendix being located in the upper right quadrant
internal hernia
intestinal loop passes through mesenteric defect, can cause strangulation/obstruction
midgut volvulus
large intestine twist over the duodenum
Omphaloenteric duct remnants
ductal remnants develop into cyst in the umbilicus or just below
- can have persistent vitelline artery
- sirenomelia
Ileal diverticulum
small out pouching of the ileum with a remnant of vitelline duct
-dark feces from upper GI bleeding
Hirschsprung disease
- aka congenital megacolon
- Neural crest cells don’t migrate properly during weeks 5-7 and the myenteric plexus doesn’t have autonomic ganglion cells
persistent cloaca
common outlet of intestinal, urinary, and reproductive tract
anorectal agenesis with rectovaginal fistula
rectum opens up into vagina
lesser omentum and falciform ligament are derived from
ventral mesentery
Primary retroperitoneals
Kidneys Adrenal glands Aorta IVC Caudal rectum Anal canal
Forgot includes and blood supply
stomach, Duodenum to just distal to the bile duct opening, liver, biliary apparatus
celiac trunk
omphaloenteric duct is obliterated by this point
week 11
midgut includes and blood supply
distal half of the duodenum, jejunum, ileum, cecum, ascending colon, and the proximal half transverse colon
SMA
hindgut
½ of the transverse colon, the descending colon, sigmoid colon, rectum, and anal canal cranial to the pectinate line
IMA
painful vs non-painful Bright red vs dark blood from hemorrhoids
Internal hemorrhoids - no pain, dark blood
External hemorrhoids - painful, bright red blood
HMG CoA reductase
rate limiting enzyme for cholesterol synthesis
SREBP
binds when low cholesterol to inc enzymes needed for cholesterol synthesis
Estradiol (E2) effects
- inhibit osteoclast -> osteoporosis
- inc metabolism -> fatigue
- Na+ and H2O retention
- vaginal cornification -> painful intercourse bc thin vaginal wall
- thin mucous (ferning)
- inc progesterone receptors
gastrin effect on bile
- directly inc bile in liver
- indirect inc by dec pH causing release of secretin (secretin inc HCO3- production in bile)
lithocolic acid
secondary bile acid that cannot be absorbed
alc effect on acetaminophen metabolism
inc P450 pathway diverting from GSH pathway
-inc in NAPQ1
zone I
zone III
zone I: glycogen and plasma protein synthesis
zone III: detox
MALE
mesospheric duct
urogenital sinus
mesospheric duct: epididymis, ductus deferens, seminal gland, efferent ductules
urogenital sinus: bladder, spongy urethra, bulbourethra, prostate (also mesenchyme)
FEMALE
paramesospheric duct
urogenital sinus
paramesospheric duct: uterus, uterine tubes
urogenital sinus: urethra, paraurethra, greater vestibular gland
Hepatocyte RER SER Gogli peroxisomes
RER: synthesis of plasma proteins
SER: biotransformatio/detox
Gogli: plasma protein and bile components
peroxisomes: oxidize FA
Dark granules
Light Granules
Dark granules: NE
Light Granules: Epi
Liver deterioration
fatty liver -> steatohepatitis -> cirrhosis -> liver failure
Barrett’s esophagus
stratified squamous -> simple columnar
Transitional zone
Peripheral zone
Transitional zone: benign hyperplasia
Peripheral zone: adenocarcinoma
OPG
osteoclast inhibiitor
Parotid
submandibular
sublingual
Parotid: serous acini cells
submandibular: serous acini cells and mucosal acini cells
sublingual: mucosal acini cells
Dentin
Enamel
Cementum
Dentin: odontoblast
Enamel: ameloblast
Cementum: cementoblast, anchors periodontal ligament to roots of tooth
