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Anatomy & Physiology II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Simple Squamous

A

-single layer of flattened cells
-fusion and filtration, not involved in protection

ex: kidney, lungs, endothelial lining of blood vessels(!!)

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2
Q

Simple Cuboidal

A
  • single layer of cube cells with large spherical central nuclei
    -secretion and absorption
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3
Q

Simple Columnar

A

-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),

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4
Q

Pseudostratified Columnar

A

-single layer of cells at different heights, nuclei is dispersed at random
-secretion, propulsion, more mucus

ex: goblet cells, airway, GI tract

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5
Q

Stratified Squamous

A

-several layers (cuboidal, columnar,squamous)
- areas that are open to outside of body

ex: upper throat area, areas subject to abrasion, vagina

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6
Q

Transitional Epithelia

A

-looks like both stratified squamous and cuboidal
-stretches

ex: bladder

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7
Q

endocrinology

A
  • communication between cells OVER DISTANCE
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8
Q

Autocrine chemical messenger

A

-Cell A releases chemical outside of cell A, but it only affects Cell A
-self regulation

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9
Q

Paracrine chemical messenger

A

-chemical secreted outside of cell A but it affects neighboring cells
-hay fever

ex: histamines

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10
Q

Neurotransmitter chemical messenger

A
  • produced by neuron
    -into synaptic cleft by presynaptic nerve terminal
    -short distance

ex: acetylcholine, epinephrine

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11
Q

Endocrine chemical messenger

A

-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

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12
Q

Major endocrine glands (AP,PP,PG,TG,PTG,AG)

A

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

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13
Q

Organs containing endocrine cells

A

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)

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14
Q

acute epinephrine

A

adrenaline
fight or flight
RR, HR go up
eyes go wide

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15
Q

Endocrine System chart

A

Amplitude moderated
concentration determines strength and magnitude

concentration equals size/strength of signal

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16
Q

Nervous system chart

A

Frequency moderated
depends on frequency of action potentials
all APs are the same size

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17
Q

Control of Hormone Release (PTH)

A

Humoral

Low Ca2+ concentration in capillary blood stimulates Parathyroid hormone (PTH).

released in response to blood levels of non-hormones: Ca2+, Na+, glucose

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18
Q

Control of Hormone Release (catecholamines)

A

Neural

Preganglionic SNS stimulates adrenal medulla to release catecholamine

fight or flight control

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19
Q

Control of Hormone Release (Tropins)

A

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

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20
Q

Negative Feedback

A

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

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21
Q

Glucose

Insulin

Glucagon

A

Blood sugar

hormone released when glucose is too high

hormone released when glucose is too low

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22
Q

Positive Feedback

A

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

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23
Q

Receptors
3 factors of specificity
receptor dynamics

A

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

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24
Q

Hormone actions on target cell (5 categories, some do all/some/none)

A

-alter plasma permeability
opens/closes ion channels

  • stimulates protein synthesis in ribosomes
  • (de)activates enzymes
  • induces secretory activity
  • stimulates mitotic activity
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25
Q

Hormone Structures
(steroid,protein, biogenic amine)

A

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

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26
Q

cAMP 2nd messenger system

A

ALL amino acid base EXCEPT Thyroid

  1. ligand hormone (1st messenger) binds to receptor (lipophobic)
  2. receptor activates G protein (Gs)
    GDP falls off, GTP is added on
  3. Gs (GTP-alpha) activates adenylate cyclase (amplifier enzyme)
  4. Adenylate cyclase converts ATP to cAMP (2nd messenger)
  5. cAMP activates protein kinase A

triggers responses from target cells

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27
Q

PIP2 2nd Messenger Systems (IP3)

A
  1. hormone binds complementary receptor
  2. G protein activates
  3. Phospholipase C enzyme activates
    (PIP2 is converted to IP3)
  4. IP3 binds to channel in endoplasmic reticulum
  5. channel opens and Ca2+ enters cytoplasm (alters enzymes or binds to calmodulin)
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27
Q

Turning off cAMP response

A

hormone falls off receptor
deactivate Gs protein by hydrolysing GTP back to GDP+ phosphate (hydrolysis)
PDE lowers levels of cAMP

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28
Q

PIP2 2nd MS (DAG)

A
  1. hormone binds complementary receptor
  2. G protein activates
    (PIP2 converts to DAG)
  3. DAG activates protein kinase
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29
Q

Steroid Hormones

A
  1. steroid hormone diffuses thru plasma and binds to intracellular receptor
  2. receptor-hormone complex enters nucleus
  3. receptor-hormone complex binds a hormone response element
  4. binding starts transcription of gene to the mRNA
  5. mRNA directs protein synthesis

ex: Lance Armstrong and the anabolic steroids, Mares and the Cyclic estrus cycle (convinces horses they’re pregnant)

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30
Q

Hormone interactions (synergistic, permissive, antagonistic)

A

work together to increase effect

gentleman effect; one lets the other go first

hormones counteract each other

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31
Q

hypothalamus and pituitary

A
  1. Neurons in the ventral hypothalamus releases hormones into primary capillary plexus
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32
Q

Oxytocin and ADH

A

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.

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33
Q

Hormones stored in neurohypophysis

A

neuronal regulations

Paraventricular: Oxytocin (contractions/ mammary glands)

Supraoptic Nucleus: antidiuretic hormone (ADH) or Vasopressin (AVP)

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34
Q

ADH
-diabetes insipidus
-breaking the seal
-hangovers

A

-neural damage leads to lack of ADH
-alc inhibits ADH
-dehydration

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35
Q

ventral hypothalamus

hypothalamic hormones

A

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

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36
Q

pituitary hormones

A

hormonal control

gigantism: GH increases BEFORE bone ossifies
acromegaly: GH increases AFTER BO
dwarfism: decreased GH, normal-ish proportions

TSH, ACTH, FSH, LH, PRL

37
Q

GH age/time/ blood levels/ stress

A

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

38
Q

Thyroid Hormones

A

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

39
Q

Synthesis of Thyroid hormone

A
  1. Iodide transported into thyroid follicle by Na+/I- symporter (needs symported bc Iodide is not lipid soluble)
  2. Thyroglobulin (Tg) synthesized in thyroid follicle
  3. Tyrosines in the Tg are iodinated by thyroid peroxidase (Tg—> Tg-I)
  4. Tg is exocytosed into follicle lumen
  5. Two iodinated tyrosines within Tg join to form T4 or T3
  6. Endocytosis of iodinated Tg into thyroid follicle cells
  7. Tg digested by lysosome enzymes into individual AA and T3/T4. AA are recycled thru thyroglobulin
  8. 3 and T4 diffuse out and enter circulatory system
40
Q

T3/T4 Regualation

A

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)

41
Q

Thyroid Effects

A

promotes normal basal metabolic rate, HR, BP, muscle function, bone growth, fertility, GI motility, female reproductive function

42
Q

Myxedema/ Hypothyroidism

A

decreases Basic metabolic rate, chillds, constipated, puffy eyes

caused by not enough Iodine uptake
myxedema is mucus swelling in the neck area

43
Q

Grave’s disease/ hyperthyroidism

A

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

44
Q

Calcium Homeostasis
-Ca2+ increased

-Ca2+ decrease

A

-calcitonin increases, PTH decreases; decreased bone absorption and Ca2+ uptake

-decreased calcitonin, increased PTH uptake; increase bone absorption, Ca2+ uptake

45
Q

Adrenal glands
(5 layers)

A

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

46
Q

Aldosterone Regulation

A

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

47
Q

Adrenal Corticosteroids

A

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

48
Q

adrenal corticosteroid imbalance:

  • addison’s disorder
  • cushing’s disorder
A

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

49
Q

3 stages of stress

A
  1. Initial fight or flight (short term stress) epinephrine, neural
  2. resistance reaction (long term stress) cortisol, hormonal
  3. exhaustion (pooped out adrenal) can lead to severe stress, beta cells in pancreas fail (insulin producing)
50
Q

Congenital Adrenal Hyperplasia

A

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)

51
Q

pancreas
-alpha
-beta

A

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

52
Q

Exercise (short term)

A

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)

53
Q

Exercise (long term)

A

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

54
Q

Diabetes Mellitus

Type I

A

“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

55
Q

Diabetes Mellitus

Type II

-diabetic ketoacidosis

A

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

56
Q

Diabetes Mellitus

Gestational Diabetes

A

pregnant women sometimes

57
Q

Hypoglycemia

A

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

57
Q

Hypoglycemia

A

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

58
Q

Pineal Gland

melatonin

A

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

59
Q

Thymus

A

lays on top of larynx, stimulates maturation of immune cells,most active in kids

thymosin
thymopoietin

60
Q

Hormone producing structures
adipose
skin
GI tract
Kidney
Heart
Placenta

A

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

61
Q

mesoderm hormones

A

produce steroids

62
Q

Blood compositions
-plasma
-buffy coat
-erythrocytes

A

Plasma is 55%
-mostly water
-albumins, globulins, fibrinogens, proteins

Buffy 1%
-Never Let Monkeys Eat Bananas
-Neutrophils, Leukocytes, Monocytes, - Eosinophils, Basophils

Erythrocytes is 44%

63
Q

Erythrocytes (RBC)

A

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

64
Q

Hemoglobin (Hb)

A

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

65
Q

Formed Elements Maturation Pathways

A

starts on hematopoietic Stem Cells

Erythropoiesis: RBC

Leucopoyesis: WBC

Platelet Genesis: thrombocytes/ platelets

66
Q

Hematopoiesis-> Erythropoiesis

A

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!

67
Q

Erythropoiesis and Erythropoietin (EPO)

A

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

68
Q

hormonal control of erythropoiesis

A

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

69
Q

Erythrocyte Life Cycle

A

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

70
Q

Erythrocyte disorder: Anemia // Thalassemia

A

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

71
Q

Erythrocyte disorder: Polycythemia

A

high red blood cell count
becomes too thick to circulate,strains heart

72
Q

Jaundice

A

liver in premature babies not fully formed; billi is accumulated

light therapy

73
Q

Leukocytes

A

immune system cells; defense
chemotaxis: chemical movement, follow chemical trail
diapedesis : squeezes thru

single or multilobed

74
Q

leukopoiesis

A

formation of white cells
all start at same origin (hemocytoblast)
become committed cells as myeloblast, monoblast, lymphoblast

75
Q

Leukocyte disorder: Leukemias

Acute leukemia

chronic leukemia

characteristics

A

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

76
Q

leukopenia vs leukocytosis

A

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

77
Q

Mononucleosis

A

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

78
Q

Platelets and Thrombopoiesis

A

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)

79
Q

hemostasis

A

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

80
Q

platelet plug formation

-von Willebrand factor
-thromboxanes
-fibrinogen

A

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

81
Q

Clot formation
-extrinsic
-intrinsic

A
  1. EXTRINSIC (chemical outside of blood)
    stimulated by thromboplastin (factor III) released by damaged tissue
  2. INTRINSIC (chemical in blood) inactive factor XII activated by coming in contact with damaged vessel
  3. 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

  1. thrombin converts fribrinogen to fibrin (the clot)
  2. thrombin activates clotting factor, promoting clot formation and stabilizes fibrin clot
82
Q

Extrinsic clotting pathways

A

chemical outside pathway
tissue factor III
Ca2+, factor X
Prothrombinase forms

83
Q

Intrinsic Clotting pathways

A

chemical part of blood
Factor XII
Activates XI
Factor X

Prothrombinase

84
Q

Factors limiting Clots

A

swift removal and dilution of clotting factors
inhibition of activated clotting factors

stops fast inactivated fast

85
Q

Factors preventing undesirable clots

A

smooth endothelial lining of blood vessels
antithrombotic substances secreted by endothelial
vit E acts as potent anticoagulant

86
Q

Disseminated Intravascular Coagulation (DIC)

A

clotting blocks intact blood vessels
severe bleeding occurs bc residual blood can’t clot
ex: pregnancy, septicemia, incompatible transfusions

bodywide

87
Q

Sympathetic ANS response to blood loss

A

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

88
Q

Clot retraction, repair, destruction

A

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

89
Q

Hemostasis Clotting disorder

thrombus
embolus
anti clotting drug

A

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

90
Q

Hemostasis Bleeding disorder

thrombocytopenia
liver failure
hemophilia
von Willebrand Disease

A

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

Anatomy & Physiology II (2 decks)

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