Exam 1 Flashcards
Simple Squamous
-single layer of flattened cells
-fusion and filtration, not involved in protection
ex: kidney, lungs, endothelial lining of blood vessels(!!)
Simple Cuboidal
- single layer of cube cells with large spherical central nuclei
-secretion and absorption
Simple Columnar
-single layer of tall cells w round OVAL nuclei
-absorption and secretion
-secretion of mucus and enzymes
-some are ciliated (part of the airway)
Ex: airway (mucus), uterine tubes (ciliated),
Pseudostratified Columnar
-single layer of cells at different heights, nuclei is dispersed at random
-secretion, propulsion, more mucus
ex: goblet cells, airway, GI tract
Stratified Squamous
-several layers (cuboidal, columnar,squamous)
- areas that are open to outside of body
ex: upper throat area, areas subject to abrasion, vagina
Transitional Epithelia
-looks like both stratified squamous and cuboidal
-stretches
ex: bladder
endocrinology
- communication between cells OVER DISTANCE
Autocrine chemical messenger
-Cell A releases chemical outside of cell A, but it only affects Cell A
-self regulation
Paracrine chemical messenger
-chemical secreted outside of cell A but it affects neighboring cells
-hay fever
ex: histamines
Neurotransmitter chemical messenger
- produced by neuron
-into synaptic cleft by presynaptic nerve terminal
-short distance
ex: acetylcholine, epinephrine
Endocrine chemical messenger
-chemicals are secreted into blood stream
-travel distance to their target
-coordinated regulation of cell function
-multiple receptors affected by cell A
ex: testosterone, thyroid, growth hormone, estrogen, etc
Major endocrine glands (AP,PP,PG,TG,PTG,AG)
Anterior Pituitary :
Posterior Pituitary:
Pineal gland: releases melatonin (sleep wake cycle)
Thyroid: produces hormone that regulates metabolic rate
Parathyroid: (behind the thyroid), regulates calcium in the blood
Adrenal: snowflakes on top of kidneys
Adrenal cortex:
Adrenal medulla: epinephrine, norephedrine
Organs containing endocrine cells
Hypothalamus:
Ventral hypothalamic hormones: stimulate/inhibit release hormones from the anterior pituitary
super optic nuclei
paraventricular nuclei
skin
thymus: regulates maturation of immune cells
heart: atria regulates blood pressure
liver: digestion control, endocrine hormones
Pancreas: 99% is digestive, 1% (endocrine) insulin and glucagon
Gonads: testes (testosterone) and ovaries (progesterone, estrogen)
acute epinephrine
adrenaline
fight or flight
RR, HR go up
eyes go wide
Endocrine System chart
Amplitude moderated
concentration determines strength and magnitude
concentration equals size/strength of signal
Nervous system chart
Frequency moderated
depends on frequency of action potentials
all APs are the same size
Control of Hormone Release (PTH)
Humoral
Low Ca2+ concentration in capillary blood stimulates Parathyroid hormone (PTH).
released in response to blood levels of non-hormones: Ca2+, Na+, glucose
Control of Hormone Release (catecholamines)
Neural
Preganglionic SNS stimulates adrenal medulla to release catecholamine
fight or flight control
Control of Hormone Release (Tropins)
Hormonal
Hypothalamus secretes hormones that stimulates anterior pituitary gland to secrete hormones (thyroid gland, adrenal cortex, gonadotropin) that stimulate other endo glands to secrete hormones
chain reaction
Negative Feedback
Anterior pituitary secretes a tropic hormone that travels to target endocrine cell through blood
The hormone from the target endocrine cell secretes a hormone to the target cell
Hormone from the target endocrine cell has neg feedback effect on anterior pituitary and hypothalamus; decreases secretion of tropic hormone
tropic hormone–> hormone–> stop tropic hormone
Ex: sweat
Glucose
Insulin
Glucagon
Blood sugar
hormone released when glucose is too high
hormone released when glucose is too low
Positive Feedback
Anterior Pituitary gland secretes tropic hormone that travels to endocrine cell
hormone from the endocrine cell travels to target cell
Hormone from the target endocrine cell has PF on anterior pituitary and increases tropic hormone release
tropic hormone–>hormone–> more tropic hormone
intensifies
ex: serotonin during birth, contractions, pressure
Receptors
3 factors of specificity
receptor dynamics
hormone levels, # receptors on target organ, affinity of hormone for receptor
up-regulation: speeds up, more receptors are created when cell binds to hormone, reduces concentration in blood
down-regulation: slows down, cell destroys receptors @ high levels, more hormones than needed, minimizes site so less hormones bind, increases concentration
Hormone actions on target cell (5 categories, some do all/some/none)
-alter plasma permeability
opens/closes ion channels
- stimulates protein synthesis in ribosomes
- (de)activates enzymes
- induces secretory activity
- stimulates mitotic activity
Hormone Structures
(steroid,protein, biogenic amine)
Steroid:
lipid soluble, adrenal cortex/gonads
Ex: cortisol
Protein: water soluble, amino acid chain
Ex: Parathyroid
Biogenic amine: water soluble EXCEPT thyroid hormone, from AA that is modified
Ex: Tyrosine
cAMP 2nd messenger system
ALL amino acid base EXCEPT Thyroid
- ligand hormone (1st messenger) binds to receptor (lipophobic)
- receptor activates G protein (Gs)
GDP falls off, GTP is added on - Gs (GTP-alpha) activates adenylate cyclase (amplifier enzyme)
- Adenylate cyclase converts ATP to cAMP (2nd messenger)
- cAMP activates protein kinase A
triggers responses from target cells
PIP2 2nd Messenger Systems (IP3)
- hormone binds complementary receptor
- G protein activates
- Phospholipase C enzyme activates
(PIP2 is converted to IP3) - IP3 binds to channel in endoplasmic reticulum
- channel opens and Ca2+ enters cytoplasm (alters enzymes or binds to calmodulin)
Turning off cAMP response
hormone falls off receptor
deactivate Gs protein by hydrolysing GTP back to GDP+ phosphate (hydrolysis)
PDE lowers levels of cAMP
PIP2 2nd MS (DAG)
- hormone binds complementary receptor
- G protein activates
(PIP2 converts to DAG) - DAG activates protein kinase
Steroid Hormones
- steroid hormone diffuses thru plasma and binds to intracellular receptor
- receptor-hormone complex enters nucleus
- receptor-hormone complex binds a hormone response element
- binding starts transcription of gene to the mRNA
- mRNA directs protein synthesis
ex: Lance Armstrong and the anabolic steroids, Mares and the Cyclic estrus cycle (convinces horses they’re pregnant)
Hormone interactions (synergistic, permissive, antagonistic)
work together to increase effect
gentleman effect; one lets the other go first
hormones counteract each other
hypothalamus and pituitary
- Neurons in the ventral hypothalamus releases hormones into primary capillary plexus
Oxytocin and ADH
Hypothalamic neurons synthesize ADH and oxytocin
Oxy/ADH transported along of hypothalamic-hypophyseal tract to posterior pituitary(stored until the neurons fire)
Oxy/ADH stored in axon terminals in posterior pituitary
Oxy/ADH released into blood when hypothalamic neurons fire.
Hormones stored in neurohypophysis
neuronal regulations
Paraventricular: Oxytocin (contractions/ mammary glands)
Supraoptic Nucleus: antidiuretic hormone (ADH) or Vasopressin (AVP)
ADH
-diabetes insipidus
-breaking the seal
-hangovers
-neural damage leads to lack of ADH
-alc inhibits ADH
-dehydration
ventral hypothalamus
hypothalamic hormones
ventral hypothalamic neurons secrete releasing and inhibiting hormones into capillary plexus
hypothalamic hormones travel thru portal veins to anterior pituitary where they stimulate/inhibit hormone release from anterior pituitary
secreted into secondary capillary plexus
hormonal regulation
GHRH- release of growth
GHIH- stops growth
TRH- acts on endo tissue
CRH- releases ACTH
GnRH- gonads
PRH- prolactin stimulatory
PIH- prolactin inhibitory
pituitary hormones
hormonal control
gigantism: GH increases BEFORE bone ossifies
acromegaly: GH increases AFTER BO
dwarfism: decreased GH, normal-ish proportions
TSH, ACTH, FSH, LH, PRL
GH age/time/ blood levels/ stress
GH levels fluctuate w age; children and adolescents have highest GH
daily fluctuations of GH throughout the day
regulated by level of nutrients in blood
certain stresses increase GH but severe stress decreases GH in children
Thyroid Hormones
Follicular cells: regulated by TSH (thyrotropin)
Thyroxine (T4): inactive form, most common secretred (2 tyrosines, 4 iodines) tissues convert T4->T3
Triiodothyronine (T3): active form (2 tyrosine, 3 iodines)
Parafollicular cells
Calcitonin: moves Ca2+ from blood to bones
Ca uptakes and osteoblasts lower Ca in blood
Synthesis of Thyroid hormone
- Iodide transported into thyroid follicle by Na+/I- symporter (needs symported bc Iodide is not lipid soluble)
- Thyroglobulin (Tg) synthesized in thyroid follicle
- Tyrosines in the Tg are iodinated by thyroid peroxidase (Tg—> Tg-I)
- Tg is exocytosed into follicle lumen
- Two iodinated tyrosines within Tg join to form T4 or T3
- Endocytosis of iodinated Tg into thyroid follicle cells
- Tg digested by lysosome enzymes into individual AA and T3/T4. AA are recycled thru thyroglobulin
- 3 and T4 diffuse out and enter circulatory system
T3/T4 Regualation
Stress and hypothermia cause TRH to release from hypothalamus into anterior pituitary
TRH causes anterior pituitary to secrete TSH passes thru the general circulation of thyroid gland
TSH increases synthesis and release of T3 and T4
T3 T4 act on target tissues to produce response
T3 and T4 have inhibitory effect on TRH secretion from Hypothalamus and TSH from anterior pituitary
(shuts off automatically)
Thyroid Effects
promotes normal basal metabolic rate, HR, BP, muscle function, bone growth, fertility, GI motility, female reproductive function
Myxedema/ Hypothyroidism
decreases Basic metabolic rate, chillds, constipated, puffy eyes
caused by not enough Iodine uptake
myxedema is mucus swelling in the neck area
Grave’s disease/ hyperthyroidism
high BMR, sweating, weight loss, exopthalmos (eyeballs protrude bc of edema in sockets), autoimmune, body produces antibody that mimics TSH action
remove thyroid and replace the hormones
Calcium Homeostasis
-Ca2+ increased
-Ca2+ decrease
-calcitonin increases, PTH decreases; decreased bone absorption and Ca2+ uptake
-decreased calcitonin, increased PTH uptake; increase bone absorption, Ca2+ uptake
Adrenal glands
(5 layers)
Capsule: fibrous connective tissue
zona glomerulosa: cells in cluster, mineralocorticoides, 95% aldosterone, mostly sodium, balances Na, bicarbonate, Cl, H ions, reduces Na excretion in urine
zona fasciculata: glutacorticoids, seen as parallel cords
zona reticularis: gonadocorticoides, glucocorticoids, looks like a net
adrenal medulla: chromaffin cells, secrete catecholamines
Aldosterone Regulation
decreased Na+ or increased K+ in blood directly stimulates zona glomerulosa in adrenal cortex, enhancing the secretion of aldosterone. Leads to increased absorption of Na+ and water , increase in BP
decreased Na+ or increased K+ in blood and decreased blood volume/ pressure prompts kidney to secrete renin initiating production of angiotensin II. Enhancing the secretion of aldosterone. Leads to increased absorption of Na+ and water , increase in BP
INCREASE in blood pressure/volume causes secretion of atrial natriuretic peptide (ANP) inhibiting aldosterone secretion in the zona glomerulosa of adrenal cortex decreasing volume/ pressure
Adrenal Corticosteroids
produced in fasciculata and reticularis; mostly cortisol
in charge of sugar balance and energy
Effects:
gluconeogenesis- production of sugar from fats and amino acids
mobilizes fat to use as energy
protein broken down for ATP or new formation of proteins
stress resistance
anti inflammatory
depresses immune functions
adrenal corticosteroid imbalance:
- addison’s disorder
- cushing’s disorder
low cortisol and aldosterone
Na is not removed from the urine, dehydration
sx: hypotension, bronze skin, weight loss
try to add from ATCH, CRH, melanin
high cortisol
high glucose, muscle and bone wasting, moon face, buffalo hump, depressed immune fxn, remove tumor
3 stages of stress
- Initial fight or flight (short term stress) epinephrine, neural
- resistance reaction (long term stress) cortisol, hormonal
- exhaustion (pooped out adrenal) can lead to severe stress, beta cells in pancreas fail (insulin producing)
Congenital Adrenal Hyperplasia
missing 1 or more enzyme needed for cortisol synthesis, partial rxn, stops production once all useful enzymes have been exhausted
decreased cortisol increases ACTH.. no negative feedback–> stimulates adrenal cortex growth
leads to enlarged adrenal glands
leftover accumulation of cortisol precursors (ingredients) which can be converted to testosterone
sx: virilization (male like sx)
pancreas
-alpha
-beta
1% endocrine
beta: produces, increases concentration of glucose in blood
liver
effects (in order): catalyse oxidation of ATP (energy output), extra glucose converts to glycogen (storage form), excess glucose becomes fate
alpha: produces glucagon which targets the liver
increase blood concentration of glucose
effects: glycogenolysis, gluconeogenesis, releases glucose into blood
Exercise (short term)
Autonomic NS tells pancreas to stop making insulin, leaves AA and glucose in blood stream until they can tell what the exercise is
Short Term exercise: sympathetic stim increases epi and glucagon
-glucagon leaves glucose in the blood
-epi increases rate of breakdown from glycogen store into glucose. Increases rate of fatty acid metabolism (muscle cells burn fatty acids)
Exercise (long term)
no longer epi driven, cortisol (long term stress), ACTH is triggered
cortisol tears down muscles into AA for fuel.
Growth hormone is released to conserve the muscle
increased reliance of fatty acids as fuel
Diabetes Mellitus
Type I
“overflow of honey”
insulin imbalance
sx: polyuria (excess urination), polydipsia (excess thirst), polyphagia (excess hunger)
TI: can’t produce insulin, don’t have the hormone to move glucose and AA to target tissue; treated w insulin (finger pricks, glucose monitor, pump, DEXCOM!)
What happens if not treated:
body is starving= stress
high levels of glucose, can be fatal
sugar shock
Diabetes Mellitus
Type II
-diabetic ketoacidosis
not enough insulin or receptors, can’t keep up with high demand of glucose release; moves some but not all glucose
-body breaks down fatty acids for fuel
pH shifts outside of normal and damages tissues
-coma XoX
Diabetes Mellitus
Gestational Diabetes
pregnant women sometimes
Hypoglycemia
low glucose in blood
hyper insulism
low blood concentration of glucose.
body triggers glucagon; shoots glucose into blood
hyperactivity, tremors, disorientation
can lead to comatose and death
bc glucose levels are too low
Hypoglycemia
low glucose in blood
hyper insulism
low blood concentration of glucose.
body triggers glucagon; shoots glucose into blood
hyperactivity, tremors, disorientation
can lead to comatose and death
bc glucose levels are too low
Pineal Gland
melatonin
response to amt of light (retina reception)
1.light enters ete stimulates APs to fire
2. APs transmitted to hypothalamus
3. APs transmitted to pineal gland sympathetic division
4. more melatonin if less light
inhibits gonadotropin releasing hormone, regulates circadian rhythm
Thymus
lays on top of larynx, stimulates maturation of immune cells,most active in kids
thymosin
thymopoietin
Hormone producing structures
adipose
skin
GI tract
Kidney
Heart
Placenta
A: leptin- satiation resistin- antagonizes insulin
S: Cholecalciferol- converts into calcitriol to help w calcium uptake; precursor to Vit D
GI: Enteroendocrine
Kidney: Erythropoetin- RBC maturation
mesoderm hormones
produce steroids
Blood compositions
-plasma
-buffy coat
-erythrocytes
Plasma is 55%
-mostly water
-albumins, globulins, fibrinogens, proteins
Buffy 1%
-Never Let Monkeys Eat Bananas
-Neutrophils, Leukocytes, Monocytes, - Eosinophils, Basophils
Erythrocytes is 44%
Erythrocytes (RBC)
Anucleate
Biconcave to increase SA
no organelles: vessel to carry oxygen
Normal Values: 5.1-5.8 mil (M); 4.25-5.25 mil (W)
Hemoglobin: 33-35% of RBC volume
Primary function: gas transport
Spectrin: flexible protein in plasma membrane
Hemoglobin (Hb)
carries oxygen, has iron in it
makes up 1/3 of RBC
4 globin chains
center of each chain has iron; binding site for Oxygen (total of 4)
Hg per L
-women 120-280g/1000mL
-men 130-280g/1000mL
O2-> lungs: oxyhemoglobin
O2-> tissues: Deoxyhemoglobim
CO2-> tissue: carbaminohemoglobin
Formed Elements Maturation Pathways
starts on hematopoietic Stem Cells
Erythropoiesis: RBC
Leucopoyesis: WBC
Platelet Genesis: thrombocytes/ platelets
Hematopoiesis-> Erythropoiesis
Hemocytoblast
Proerythroblast (committed cell) has nucleus that has not specialized yet
Developmental pathway:
P1: Ribosome synthesis (early erythroblast)
P2: hemoglobin accumulation (late erythroblast)
normoblast
P3: ejection of nucleus (reticulocyte)
Erythrocyte!
Erythropoiesis and Erythropoietin (EPO)
low blood oxygen causes the kidneys to produce EPO, the increased EPO triggers red bone marrow to speed up RBC production, leading to increased blood oxygen
humoral
hormonal control of erythropoiesis
effects of EPO
-more rapid maturation of committed bone marrow cells
-increased circ reticulocyte count in 1-2 days
testosterone also enhances EPO production, resulting in higher RBC count in males
long term drawback: Blood gets thicker makes it harder to pump
Erythrocyte Life Cycle
Life span: 120 days
Aging: becomes brittle/ damaged; the plasma membranes can rupture
Destruction/ Recycling:
macrophages: engulf old or damaged RBC
iron: is bound to a protein otherwise can be toxic
Heme: iron removed leaving billirubin
Globin: broken down into its AA form used by body
Erythrocyte disorder: Anemia // Thalassemia
low concentration of oxygen due to various reasons
hemorrhagic: injury, bleeding, ulcer, hemorrhoids
Hemolytic: prematurely lysed RBC (malaria, blood parasites, toxins)
Aplastic: inhibition, bone marrow destruction (cancer, cancer treatment, toxins)
Iron deficiency
Pernicious: Vitamin B12 deficiency
Sickle Cell: sickle shaped RBC (malaria)
Thalassemia: mediterranean descent; Hb deficiency, transfusions are needed
Erythrocyte disorder: Polycythemia
high red blood cell count
becomes too thick to circulate,strains heart
Jaundice
liver in premature babies not fully formed; billi is accumulated
light therapy
Leukocytes
immune system cells; defense
chemotaxis: chemical movement, follow chemical trail
diapedesis : squeezes thru
single or multilobed
leukopoiesis
formation of white cells
all start at same origin (hemocytoblast)
become committed cells as myeloblast, monoblast, lymphoblast
Leukocyte disorder: Leukemias
Acute leukemia
chronic leukemia
characteristics
named according to which cell it involves
AL: advances rapidly, mostly affects young children, affects earliest stage of Leukopoiesis… no healthy cells are created
CL: ending stages of leukopoiesis, usually affects elderly pts, slow generation
immature nonfunctional WBC
bone marrow full of cancerous leukocytes
death: internal hemorrhage, infection
treatment: radiation, chemo, bone marrow transplant
leukopenia vs leukocytosis
leukopenia is decreased # of cells
increases risk of infection
Leukocytosis is the slight increase of leukocytosis
usually due to recent infection
measure each type of cell and compare to “never let monkeys eat bananas” and their appropriate %ages
Mononucleosis
caused by Epstein Barr virus
excessive number of atypical WBC (there’s a lot of funny looking WBCs)
fatigue, swollen nodes, sore throat, fever
no cure, let it run its 3-4 wk course
Platelets and Thrombopoiesis
blood clotting
unused platelets are kept “unsticky” with nitric oxide
platelets become sticky when activated by damaged vessels
250-500,000 per cubed millimeter of blood (mm3)
hemostasis
fast rxns to stop bleeding:
vascular spasms: muscles contract, pushes in the hole to slow down blood loss
platelet plug formation: plugs up the hole, is placeholder until the tissue regenerates
coagulation
platelet plug formation
-von Willebrand factor
-thromboxanes
-fibrinogen
platelet adhesion starts when von willebrand factor stick connect to collagen and platelets
during platelet release, ADP, thromboxanes release to activate other platelets (chain platelets)
platelet aggregation happens when fibrinogen receptors on activated platelets connects to fibrinogen, connecting platelets to each other… forming a platelet plug
Clot formation
-extrinsic
-intrinsic
- EXTRINSIC (chemical outside of blood)
stimulated by thromboplastin (factor III) released by damaged tissue - INTRINSIC (chemical in blood) inactive factor XII activated by coming in contact with damaged vessel
- activation of EITHER path results in activated factor X production
4.Activated factor X, factor V phospholipids and Ca2+ form prothrombinase
5.prothrombinase converts prothrombin to thrombin
- thrombin converts fribrinogen to fibrin (the clot)
- thrombin activates clotting factor, promoting clot formation and stabilizes fibrin clot
Extrinsic clotting pathways
chemical outside pathway
tissue factor III
Ca2+, factor X
Prothrombinase forms
Intrinsic Clotting pathways
chemical part of blood
Factor XII
Activates XI
Factor X
Prothrombinase
Factors limiting Clots
swift removal and dilution of clotting factors
inhibition of activated clotting factors
stops fast inactivated fast
Factors preventing undesirable clots
smooth endothelial lining of blood vessels
antithrombotic substances secreted by endothelial
vit E acts as potent anticoagulant
Disseminated Intravascular Coagulation (DIC)
clotting blocks intact blood vessels
severe bleeding occurs bc residual blood can’t clot
ex: pregnancy, septicemia, incompatible transfusions
bodywide
Sympathetic ANS response to blood loss
more than 10% lost:
increases vasoconstriction, increases HR and contractions
redistributes blood to heart and brain
can keep bp up until 40% blood is lost
Clot retraction, repair, destruction
Clot retraction:
30-60 mins
actin & myosin
serum evacuates
pulls wound in together
repair:
PDGF: platelet derived growth factor
fibroblasts: connective tissue patch
vascular endothelial growth factor: rebuilds endothelial lining
destruction:
plasminogen: woven into the clot
plasminogen activator: converts plasminogen into plasmin
plasmin: dissolves the clot
Hemostasis Clotting disorder
thrombus
embolus
anti clotting drug
T: stationary clot, forms in wrong location
(coronary thrombus)
E: Moving clot (heart attack, stroke, pulmonary embolism)
ACD:
aspirin- inhibits thromboxane for men it prevents further heart attack and women it prevents stroke
heparin- surgical grade
warfarin- rat poison
Hemostasis Bleeding disorder
thrombocytopenia
liver failure
hemophilia
von Willebrand Disease
T: less than 50,000/mm3 caused by suppression or destruction of bone marrow
L: where factors are made
H: deficiency in clotting factors, sex linked
vWD: missing factors make platelets stick
