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5 types of leukocytes
neutrophils
eosinophils
basophils
monocytes
lymphocytes
Two categories of immune defence
innate (nonspecific) immunity and adaptive (specific) immunity
Four types of innate immunity
kills by:
inflammation
interferon
natural killer cells
complement system
Goal of inflammation
bring phagocytic cells, fluid and plasma proteins to the affected area to
-kill microorganisms
-remove debris
-prepare tissue for healing
Inflammatory response
activation of macrophages- phagocytosis, cytokines
Histamine release from mast cells- vasodilation’
increased capillary permeability (due to histamine and cytokines)- edema, pain, clotting
Leukocyte migration (monocytes and neutrophils)
phagocytosis of bacteria and debris (macrophages and neutrophils) (produces pus: leukocytes and digested tissue)
Abscesses
swollen mass filled with pus
boils
abscess with hair follicle
how do immune cells kill bacteria
Immune cells make hydrogen peroxide (like in the brown bottle) and convert it into even deadlier chemicals like bleach to destroy trapped bacteria.
bacteria at injury site are
exogenous pyrogens
phagocytic secretion s are
endogenous pyrogens
symptoms of inflammation
fever
how do endogenous pyrogens cause fever
the pyrogens go to the hypothalamus which stimulates prostaglandin release and increases the body’s thermostat
Pyrogens effect on temp
they don’t just cause increase in temp, they change your brain’s thermostat to a new baseline temp
NSAID
decrease inflammation by inhibiting the production of prostaglandins which lead to fever and histamine.
interferons
virus control
innate, nonspecific defense system
interferes with viral replication
interferon function
infected cell produces interferon which passes it to its neighbors and triggers production of enzymes that prevent protein synthesis and break down of viral RNA so virus can invade but can’t control the cell
Viral lytic cycle
virus injects nucleic acid into the bacterial cell and its replicated and new virus is produces and released
TSH
stimulates secretion of thyroid hormones
stimulates growth of thyroid gland
Regulation of TSH
stimulated by TRH
inhibited by thyroid hormone
Thyroid hormone synthesis
Thyroid hormone synthesis begins in the follicular cells, where thyroglobulin (TG) is produced and secreted into the colloid. There, tyrosine residues on TG are iodinated to form MIT (monoiodotyrosine) and DIT (diiodotyrosine), which couple to form T3 (MIT + DIT) and T4 (DIT + DIT), still attached to TG. This iodinated TG is then endocytosed back into the follicular cell. When TSH from the anterior pituitary binds to its receptor on the cell membrane, it activates a cAMP-protein kinase pathway, which stimulates this endocytosis process. Inside the cell, lysosomes fuse with the vesicles containing TG-T3 and TG-T4 and cleave the hormones from TG. Finally, free T3 and T4 are released into the bloodstream, where they travel to target tissues to regulate metabolism.
T3 vs T4
T4 is more common
T3 more active
Thyroid hormone actions (2)
increases metabolic rate and heat production by increasing sympathetic activity
stimulates protein synthesis and growth (stimulation of GH)
Thyroid hormone secretion regulation
stimulated by TSH
control of thyroid hormone secretion
high levels of t4 inhibits TRH
Hypothyroidism
iodine deficiency
deficiency of TRH and or TSH
cretinism
hypothyroidism in youth
myxedema
hypothyroidism in adults
endemic Goiter due to iodide deficiency
With low dietary iodide, thyroid hormone synthesis decreases- less negative feedback and an increase in TSH causing thyroid to enlarge
Hyperthyroidism
autoimmune production of thyroid stimulatingimmunoglobulins- antibodies against TSH receptors on thyroid
thyroid is stimulated but no negative feedback
little calcium
hypocalcemia
too much calcium
hypercalcemia
Control of extracellular calcium
thyroid- calcitonin- uptake of calcium into bones
Parathyroid- PTH- release of CA into blood
Vitamin D is activated by
sunlight
Regulation of calcium levels
Vitamin D and PTH
calcitriol to kidneys—reduce excretion, small intestine- increase absorption
Adrenal cortex is
steroids
adrenal medulla is
catecholamines (Epi and NE)
The adrenal medulla is made of modified post-ganglionic sympathetic neurons that release catecholamines—mainly epinephrine (80%) and some norepinephrine (20%)—into the bloodstream. This hormone release is controlled entirely by the sympathetic nervous system to help the body respond to stress.
Epinephrine’s effects on fuel metabolism (5 things)
Ach causes release of EP which
breaks down triglycerides into free fatty acids
breaks down glycogen in muscle into lactate
breaks down glycogen in liver into glucose
increase glucagon release
decreases insulin release
Pheo
adrenal tumor- Heightened sympathetic response
triggered by: physical exertion, anxiety, bowel movement
Cortisol
increases blood glucose
increase protein and fat use
regulation of cortisol
stimulated by corticotropin realeasing horomone from hypothalamus and adrenocorticotropic hormone from the anterior pituitary
Cortisol is effected by what two factors
stress and circadian rhythm
cushings disease: cortisol hypersecretion
too much cortisol, increased bllood sugar, fat deposits, muscle weakness, buffalo hump, stretch marks, poor wound healing, mental deficiencies
precursor for all steroid hormones
cholesterol.