AP Endocrine Quiz

H2O Soluble hormones

NOT bound to a protein

• short ½ life bc unbound

Lipid Soluble hormones

Bound to proteins in blood

• When bound, hormones are inactive and are reservoirs

Up regulation

Increase number of receptors, caused by low amt of hormones

Down regulation

Decrease receptors, caused by alot of hormones

Growth Hormone (somatostatin)

inc fat breakdown/protein synthesis/raises blood glucose levels

• inc secretion of insulin like growth factors

• Released from ant pit when stim by GHRH from Hypothal

Thyroid Stim Hormone (Thyrotropin)

causes inc production/release of TH

• TSH and TSH released when blood TH levels are low

Adrenocorticotropic hormone

• increases production of steroid hormones from adrenal cortex from stress (cortisol)

• stress/exercise/low BG—hypothal inc Corticotropin RH—anti pit releases ACTH—inc prod steroid horm

Gonadotropin hormones

hypothal releases GnRH—ant pit releases FSH and LH

How thyroglobin (colloid) leaves follicle cells

enters fol cell—converted to T3/T4—leave cell and enter caps—in blood bound to plasma proteins (when unbound to binds to receptors and causes protein synthesis)

Causes of hypothyroidism

Iodine deficiency, too little/too much TSH, thyroid storm , graves disease

Parafollicular cells (C-cells)

secrete calcitonin—released when Blood calcium levels are too high (inhibits osteoclasts)

Parathyroid Glands

Secrete PTH—release it when blood Calcium levels are too low (inhibits osteoblasts), converts Vit D intoactive form for Ca abs

• No Parathyroid gland=hypocalcemia (causes Na channels in CM to open which keeps cells depolarized)

Adrenal Medulla

Nervous Tissue

• Releases NE and Epinephrine when stim by symp NS (inc HR and vasoconst BV in GI, skin surface)

• Epinephrine: inc Blood glucose effects by stim glycogen breakdown (dec insulin sec)

Adrenal Cortex

Glandular Tissue

• Releases Aldosterone and Cortisol in response to ACTH

Mineralocorticoids

made by zona glomerulosa in Adrenal Cortex

• Aldosterone is released in response to ACTH

Glucocorticoids

Made in zona fasciculata in Adrenal cortex

• Cortisol release in response to ACTH

Cortisol effects

1. Gluconeogenesis

2. Develop receptors on epinephrine and norepinephrine cells

3. suppress immune system

Gonadocorticoids

made by zona reticularis in adrenal cortex

• Androstenedione: male secondary sex characteristics

Endocrine cells

Islets of Langerhans cell types:

1. Alpha cells- secrete glucagon

2. Beta cells- secrete insulin

3. Delta cells- secrete somatostatin (GHIH)

Seminal vesicles

70% of semen

• has prostaglandins for uterine contraction

• high in fructose and citric acid

Prostate gland

30% semen

• inferior to bladder

Sertoli cells/what they secrete/what hormone targets it

walls of seminiferous tubules, extend from BM to lumen

• forms tight junction to make blood-testis barrier

• secrete inhibin and androgen binding proteins

• FSH targets Sertoli cells and causes them to release ABP

Leydig cells

between seminiferous tubules

• LH causes them to secrete testosterone

oocyte

egg before it finishes meiosis

Follicle

oocyte+follicle cells

Antrum (follicular cavity)

Cavity that forms between follicle cells (cells surrounding oocyte)

• mature/Graafian follicle when the cavity forms

Cumulus oophorus

follicle cells closest to oocyte

What happens during ovulation?

Oocyte and cumulus oophorus break through ovary wall and leave rest of follicle behind in the ovary which form the corpus luteum

Corpus luteum

leftover follicle in ovary the oocye leaves behind during ovulation

• secretes estrogen and progesterone

Gestation

pregnancy from last period to birth

Morula

stage when ball of cells is 16 or more

Blastocyst

when a cavity forms in embryo bw 2 cell populations (embryoblast and trophoblast)

Embryoblast

future embryo and source of extraembryonic membranes

Trophoblast

forms part of placenta

What hormone does the developing placenta secrete to prevent menstruation?

Human chorionic gonadotropin- keeps corpus luteum in the ovary to secrete estrogen and progesterone

Extraembryonic membranes made by the Embryoblast

1. Amnion- fluid

2. Yolk sac- BV for digestion

3. Allantois- umbilical veins linking embryo to mother

4. Chorion- forms from trophoblast, becomes embryos part of placenta

Epiblast

inner cell mass, flat oval disk

Gastrulation

forming 3 primary germ layers in embryo

Primitive sheet

cells in epiblast move to center and form a long ridge called prim sheet

Endoderm

first layer to form during gastrulation

• lines resp and digest sys

Mesoderm

second layer to form during gastrulation

• muscle and connective tissues

Ectoderm

cells that dont migrate during gastrulation

• epidermis of skin and nervous system

Ductus Arteriosus

passage b/w pulm trunk and aorta (before birth)

Ductus Venosus

part of umb cord below liver

• blood goes from IVC to RA (has oxygen from mother bc lungs cant be used yet)

What does somatostatin inhibit the release of?

• Also know as GHIH

• inhibits insulin, glucagon, and GH

• secreted by delta cells of endocrine glands in pancreas

• Also inhibits stomach secretions

Order of filtration from glomerulus through Bowmans capsule

Glom-sim squam epith w/fenestrae- thin BM- podocytes w/ filt slits (visceral)- sim squam epith (parietal)

Juxtaglomerular Apparatus

Cell between afferent arterioles and distal conv tubule

• secretes renin (inc BP)

• Involved in tubuloglomular feedback (chem sig from macula densa cells of loop sent to afferent arterioles)= slow urine flow/low nacl conc dialates afferent art and secretes renin)

Autoregulation

local control

• Afferent art const/relax in response to Myogenic mechanism (bodys BP rise, art constricts) and tubuloglomerular feedback (

How Na goes from filtrate to BV

Na goes in cell down conc grad-pumped out using NaK pump-water folloes using symport via aquaporins

Renin-Ang-Aldosterone Mechanism

Renin secreted by JGA when BP dec- converts angiotensin to angiotensin 1- ACE converts Angiotensin 1 to angiotensin 2- angiotensin 2 inc BP and releases aldosterone and ADH

Where does Renin come from?

JGA cells of nephrons

Where does angiotensin 1 come from?

Liver

Where does Aldosterone come from?

Adrenal gland

Where does ADH come from?

Hypothal of brain (pituitary)

Where does Atrial Natriuretic hormone come from?

Cardiac muscle cells

GI tract layers

1. Mucosa: epith-lamina propria-muscularis mucosae

2. Submucosa: Meissner/submucosal plexus(stim gland sec), part of enteric NS

3. Muscularis: inner circular-Auerbach/myenteric plexus(peristalsis/pacemaker)-outer longitudinal

4. Seros/adventitia

Enteric NS

in GI tract wall, local control

• submucosal+myenteric plexuses

• “gut brain”

Mesogaster

mesentery that attaches to stomach (gaster)

Mesentery Proper

mesentery attached to SI (enteron)

Parotid glands

Saliva is mostly serous fluid

Submandibular gland

saliva is serous fluid+mucous

Sublingual glands

Saliva is mostly mucous

Cells lining gastric glands

1. Mucous Neck cells: secrete mucus

2. Parietal cells: produce HCl and intrinsic factor (helps vit B get abs)

3. Chief cells: produce pepsinogen

4. Endocrine cells: produce hormones (gastrin)

• Pepsinogen+HCl=Pepsin (active, starts protein digestion)

Gastric Secretion Phases

1. Cephalic phase: thinking about food

• Vagus releases ACh-causes stomach to release gastrin and histamine BEFORE food enters (releases gastric juice)

2. Gastric Phase: food in stomach

• stretch triggers mechanoreceptors

• vagus still releases ACh like above

3. GI Phase= slow down phase, duodenum doesn’t like low pH

• most fat digests in duodenum

• chyme entering duodenum triggers mechanoreceptors which causes enterogastric reflex to reduce gastric secretion

Acidic chyme in duodenum causes relase of?

Secretin- inhibits gastric secretions and causes liver to secrete bile

Fatty chyme in duodenum causes release of?

CCK- inhibits gastric secretion

SI mucosa/cell types

Simple columnar epithelium

1. Absorption cells

2. Goblet cells: mucus

3. Endocrine cells: produce CCK/secretin

4. Granular cells: immune function (paneth cells)

• Endocrine and granular cells are at bottom of crypts of Lieberkuhn

Liver Lobule parts

Hepatic cords: made of hepatocytes

Hepatic sinusoid: where A and V blood mix

Bile Canaliculi: b/w hepatic cords, feed into small bile ducts

• Between hepatic cords can either be sinusoids or bile canaliculi

Bile production/purpose

made by hepatocytes in liver and released into bile canaliculi

• Bile salts break lipids into smaller drops so lipase can digest them easier

• Bile neutralizes acidic chyme from stomach

• Secretin causes liver to secrete bile

Hepatic macrophages (Kupffer cells)

phagocytize worn out BC and bacteria, in liver

When does gall bladder release bile?

In response to CCK from duodenum

What happens when there is acidic chyme in duodenum?

acidic chyme-secretes secretin (causes liver to secrete bile)-panc duct cells release buffer soln-raises duod pH

What happens when there is fatty chyme in duodenum?

fatty chyme-secretes CCK (causes GB to release bile)- panc acinar cells release enzymes

Epithelium of anal canal?

transitions from simple columnar to strat squam

What promotes digestion?

Parasym sys, CCK, gastrin

Carb digestion

glucose symported in with Na-fac dif out-enter cap-go to liver via HPV-converted to glycogen or used

Lipid digestion

broken into monoglyc+FA; bile salts surround it to form micelles; lipids enter cell simple dif; converted to triglycerides; proteins coat trig to form chylomicrons; extic exocytosis and go to lacteal

Protein digestion

enter epith cells using Na; broken into AA; leave and enter cap and go to liver

Ventricle Systole

Ventricles contract- pressure closes AV valves but not great enough to open semilunar valves

Early Ventricle diastole

• follows T wave

• Ventricles relax

Isovolumetric relaxation

all valves are closed and blood starts entering atria

Aortic Pressure

Blood pressure

120- aorta pressure when contracting

80- aorta pressure when relaxed

Mean Arterial Pressure

= Cardiac Output (CO) times Peripheral resistance (PR)

Systolic+Diastolic Average

Peripheral resistance

sum of effects of vessel diameter (des res), vessel length (inc res), and blood viscosity (inc res)

Cardiac Output

amount of blood pumped by heart in one min

CO=HRxSV (stroke volume)

Stroke volume

volume of blood pumped out of heart in one beat

Why does exercise increase HR?

1. inc lung inflation stims stretch receptors and sends message to cardoreg center- tells symp sysy to inc HR

BV layers/tunics

1. Tunic intima= endothelium

2. Tunic Media= smooth muscle for const/dia

3. Tunic adventitia/externa= mostly CT

Do arteries or veins have a thicker tunic Media?

Arteries

Artery types

1. Elastic= largest diameter, elstin fibers, walls stretch

2. Muscular= more smooth muscle, vasoconstriction/dialation

3. Arterioles= smallest art where tunics can be ID, does most of the vasoconstriction/dialation!!!

What helps pump blood in veins back to heart?

1. valves to prevent backflow

2. skeletal muscle outside

3. Neg pressure from diaphragm

Precapillary Sphincters

reduce blood flow to region

Thoroughfare channels

link arterioles to venules when precapillary sphincters are closed

Capillary leakiness types

1. Continuous= no gaps bw endothelial cells (muscle)

2. Fenestrated= endoth cells have thin fenestrae (intestines)

3. Sinusoidal= largest gap diameter (endocrine glands to get hormones into blood)

Arteriole vs Venous end of caps

Arteriole: high O2, high BP, high nutrients, low CO2

IF at art end: low O2, high CO2, high waste, low nutrients

Venous: low O2, high CO2, low BP, high waste

IF at ven end: high O2, low CO2, high nutrients, low waste

What pushes fluid out at the arteriole end?

Hydrostatic pressure

What causes fluid to re-enter venule end and go back into blood?

Osmotic pressure

Laminar vs Turbulent flow

Laminar= fastest blood flows in center (when flow resumes, diastolic)

Turbulent= anything that disrupts flow (first sounds when taking BP, systolic pressure, makes Karotkoff sounds)

Types of plamsa proteins

1. Albumins= maintain blood colloid osmotic pressure

2. Globulins= immune response

3. Fibrinogen= make fibrin for blood clots

Erythrocyte formation

Proerythroblasts-erythroblasts (lose nucleus)- reticulocytes (lose ribosomes)- mature RBS