PHYSI Flashcards
Plasma Protein: Globulins
Clotting, antibodies
Plasma Protein: Albumins
Coloid osmotic pressure
Plasma Protein: Fibrogen
Forms fibrin -> blood clotting
Plasma Protein: Transferrin
Iron transport
Tron from diet
Absorbed -> bind to transferrin in the blood plasma -> transport to the bone marrow -> RBC production.
Iron storage
Liver -> stored as ferritin
RBC destruction
Spleen
Granulocytes
Basophils, eosinophils, neutrophils
Basophils
Large blue granules
Release histamine and heparin -> inflammation
Eosinophils
Pink staining granules
Allergic reaction + parasitic disease
Cytotoxic cell type -> release granules which attach to cell and damage/kill
Neutrophils
Multi-lobed nucleus
Phagocytic -> ingest bacteria
Release cytokines
Monocytes
Circulate in blood -> enter tissue and mature into macrophages
Lymphocytes
B cells (antibodies) T cells ( cytotoxic cells) Natural killer cells (NK cells)
Sry genes
Cause development of sertoli and leydig cells
Sertoli cells
secrete anti-malariant hormone -> block female development
Leydig cells
Produce testosterone
Male Reproductive Tract
Testis -> deposit material into the epididymis -> corder = section of epididymis where sperm is stored -> ductus deferens -> ejaculatory ducts -> urethra -> glans penis
The testes
Seminiferous tubules = formation of sperm
Extra tubular stroma = contain leydig cells -> testosterone production.
GnRH
Released by hypothalamus -> stimulates gonatotropic cells of the anterior pituitary -> FSH and LH release
FSH
Targets sertoli cells -> maintain spermatogenesis
Release inhibin -> -ve feedback to anterior pituitary
LH
Stimulate Leydig cells -> testosterone production
Testosterone = -ve feedback to inhibit GnRH and LH release
Epididymis
Sperm in testes not mature -> develop maturity in the epididymis
Caput -> corpus -> cauda
2 cell 2 gonadotrophin hypothesis
Thecal cells: stimulated by LH -> produce androgens
Granulosa cells: stimulated by FSH -> produce oestrogens.
FSH
Stimulates follicles to grow
Ovulation
Oestrogen dominates the first stage of the menstral cycle and progesterone dominates the second. Mid point (approaching ovulation) -> oestrogen levels increase -> -ve feedback switches to +ve feedback -> GnRH release -> LH surge -> ovulation
Oral Contraceptive Pill
High progesterone + oestrogen levels
Do not get ovulation -> LH surge stopped
Reduce FSH -> follicles stopped from developing
Puberty
GABA release -> suppress GnRH receptors -> loss of GABA system during adolescence.
Menopause
Increased gonadotrophins
Loss of LH and FSH
Fast block - egg fertilization
Na influx -> changes membrane potential (depolarisation)
Slow block - egg fertilization
Intracellular release of Ca -> rigid membrane and removes proteins which sperm binds to
Re-initiates meiosis
Early Pregnancy
HCG produced -> stimulates the corpus luteum to produce progesterone and oestrogen -> supresses GnRH, LH and FSH -> dont want another egg being released.
Mid/late pregnancy
Corpus leuteum produces oestrogen and progesterone for 7-10 weeks and then placenta then starts to secrete its own. -> reduction of HCG
Progesterone: blocks contraction
Oestrogen: stimulates mammary gland development.
Parturition
Placenta -> produce CRH -> induce contractions and primes prostaglandins (further contractions)
Oxytocin released by posterior pituitary
Gastrointestinal Tract Control
By the enteric nervous system which is a part of the autonomic nervous system.
Parasympathetic Innervation
From the CNS
- From medulla and runs into the vagus nerves
- From sacral spinal cord and runs into the pelvic nerves
Sympathetic Innervation
Arise in the spinal cord
Form synapses in superior cervical postganglionic cells projecting into the gut.
Long Reflexes
Integrated into the CNS -> originate in the gastrointestinal tract or enteric nervous system.
Short Reflexes
Originate in the enteric nervous system and are carried out entirely within the wall of the gut.
Blood leaves the heart via
the abdominal aorta
Blood leaves the gastrointestinal tract via
the hepatic portal vein
Saliva Gland - parotid
Serous secretion
Saliva Gland - Submandibibular
Mainly serous with some mucosal
Saliva Gland - Sublingual
Mainly mucous
Saliva Ducts
Impermeable to water
Na and Cl absorbed
K and HCO3 secreted
Preparatory phase of swallowing
Bolus formed and lubricated during cewing
Oral phase of swallowing
Bolus propelled into the pharynx by the tongue
Pharyngeal phase of swallowing
Peristaltic wave begins
Soft palate elevates and seals the nasopharynx
Epiglottis tilts downwards
Esophageal phase of swallowing
Upper oesophageal sphincter closes
Lower oesophageal sphincter relaxes
Peristalsis propelles bolus into the stomach
HCL
Activate pepsinogens
Intrinsic Factor
Absorption of dietary vitamin D
Pepsinogen
Active when exposed to gastric juices
Inactive in the duodenum
Parietal Cells
Secrete acid
Chief Cells
Secrete pepsinogen
G Cells
Secrete gastrin -> act on ECl cells and parietal cell.
ECL releases histamine
Increase acid secretion by the parietal cell
Cephalic Phase of Acid Secretion
thought, sight, smell, taste, chewing of food
30%
Gastric Phase of Acid Secretion
Distension of the stomach, prescence of AA and peptides
60%
Intestinal Phase
10%
Chyme moves into the dudeum
Detection of protein = increase secretion by chief and parietal cells
Detection of fat + acid = -ve feedback to decrease secretion by chief and parietal cells
Point where live, gall bladder and pancrease enter the duodenum
Spincter of Oddi
Pancreas
Secretes digestive enzymes and neutralises acid.
Acid in duodenal lumen
S cells detect acid -> release secretin -> act on duct cells in the pancreas -> release bicarbonate
Fat in the duodenal lumen
I cells detect fat -> secrete CCK -> act on acinar cells in the pancreas -> release digestive enzymes
Bile Secretion
Fat detected by I cells -> release CCK -> cause relaxation of sphincter of oddi -> gall bladder contracts -> bile ejected into the bile duct
Osmolality
Osmo/kg
Osmolarity
osmo/L
Cortical Nephrons
Most of structure in cortex and a short loop of henle
Juxtamedullary Nephrons
Located next to medulla and cortex boarder
Long loop of Henle
Podocytes
Cells which make up Bowman’s capsule
Filtration Slits
Spaced between podocytes
Fenestration
Holes between endothelial cells in glomerular capillary
Hydrostatic pressure in glomerular capillary
Drives filtration
Hydrostatic pressure in Bowman’s capsule
Acts against filtration
Colloid Osmotic pressure in glomerular capillary
Acts against filtration
Colloid Osmotic pressure in Bowman’s capsule
Close to 0
Proteins mostly -ve charge and fail to cross the membrane
Intrinsic Regulation of GFR
Myogenic regulation and tubuloglomerula regulation
Myogenic regulation
Increase in BP = stretch of afferent arteriole -> detected my muscle cells -> release of Ca -> vasoconstriction of afferent arteriole -> decrease in GFR
Tubuloglomerula regulation
Tuble goes through arterioles -> detects the amount of Cl inside the cells
If there is an increase in Cl adenosine is released with causes vasoconstriction of the afferent arteriole -> decrease in GFR
Increase solutes in thick ascending limb
Detected by macula densa cells -> secretion of adenosine -> constriction of afferent arteriole -> decrease GFR
Decrease solutes in thick ascending limb
Nitric oxide secretion -> dilation of afferent arteriole -> increase GFR
Extrinsic Regulation of GFR
Neural Regulation, adrenalin, renin/argiotension/aldosterone
Neural Regulation of GFR
Baroreceptors detect decrease in BP -> sympathetic nerves case vasoconstriction of afferent arteriole -> decrease in GFR -> more absorption -> increase in BP.
Adrenalin regulation of GFR
Act on adrenergic receptors on afferent arteriole -> vasoconstriction -> decrease urine output during time of stress
Renin/argiotension/aldosterone regulation of GFR
Low BP -> renin secreted -> angiotension I -> angiotension II -> vasoconstrictor -> decrease in GFR
Proximal Tubule
AA and glucose reabsorbed
Amount of water reabsorbed = amount of solutes reabsorbed -> no net change in the osmolality of the filtrate.
Sodium co-transporters transport glucose and AA into the cell.
Descending Loop of Henle
Not permeable to solutes -> only water reabsorbed
Increase in osmolality
Thick Ascending Loop of Henle
Impermeable to water
Re-absorption of solutes
Na-K-Cl co-transporter
Build up of -ve charge allows +ve solutes to move through the tight junctions between cells.
Early Distal Tubule
Impermeable to water
Re-absorption of solutes
Na-Cl co transporter
Late Distal Tubule and Collecting Duct
Reabsorption of Na and water and secretion of K
Principle and intercalated cells
Low BP and high K causes release of aldosterone -> more pumps produced
Water Permeability of the LDT and CD
Increase in blood osmolality -> osmos receptors -> ADH secretion -> binds to cell -> adenylate cyclase -> cAMP -> PKA -> more aquaporins in membrane -> more water absorbed. k