First Aid

ENDOCRINE SYSTEM
1) The endocrine system comprises widely distributed organs that work in highly integrated
manner to _____________ a state of ____________ within the body.
a) hormonal equilibrium
b) Hormonal Lesion
c) orchestrate
d) Both a and c
2) Endocrine diseases can be classified either as diseases of underproduction or

overproduction, or as conditions involving the ______________which themselves may be
associated with underproduction or overproduction of hormones.
a) development of muscle lesions
b) development of glands lesions
c) development of hormone lesions
d) development of mass lesions
3) Thyroid diverticulum arises from floor of primitive_________ and descends into neck.
a) Pharynx
b) Larynx
c) Esophague
d) Oropharynx
4) Connected to tongue by ____________ duct, which normally disappears but may persist as
cysts or the pyramidal lobe of ______________.
a) Hypogossal and Hypothroid
b) Hypothyroglossal and thyroid
c) Thyroglossal and thyroid
d) Hypergossal and Hypothyroid
5) Foramen ____________ is normal remnant of _______________duct.

a) Cecum and Hypogossal
b) Cecum and thyroglossal
c) Hypogossal and Cecum
d) Thyroglossal and Cecum
6) Most common _________ thyroid tissue site is the tongue (lingual thyroid).
a) Mesopic
b) Endopic
c) Ectopic
d) Hydropic
7) Removal may result in hypothyroidism if it is the only thyroid tissue _________.

a) Present
b) Absent
c) None of above
8) Thyroglossal duct cyst A presents as an __________ midline neck mass that moves with
swallowing or protrusion of the tongue.
a) Anterior
b) Posterior
c) Lateral
d) Medial
9) Thyroglossal duct cyst:
a) ( persistent cervical sinus leading to pharyngeal cleft cyst in lateral neck).

b) ( persistent Lumbar sinus leading to pharyngeal cleft cyst in lateral neck).
c) ( persistent Lumbar sinus leading to pharyngeal cleft cyst in Medial neck).
d) ( persistent cervical sinus leading to pharyngeal cleft cyst in Medial neck).
10) _____________Cells and _____________ cells (aka, C cells, produce Calcitonin) are derived
from _______________.
a) Thyroid cell and Parathyroid cell and Endoderm
b) Thyroid follicular and Parafollicurlar cell and Ectoderm
c) Thyroid follicular and Parafollicurlar cell and Entoderm
d) Thyroid cell and Parathyroid cell and Ecdoderm
11) Adrenal cortex and medulla: Adrenal cortex (derived from _________) and medulla (derived
from ___________).
a) Mesoderm and Neural Crest
b) Neural Crest and Mesoderm
c) Endoderm and Neural Crest
d) Ectoderm and Neural Crest
12) GFR corresponds with

a) Salt (mineralocorticoids), Sugar (glucocorticoids), and Sex (androgens).
b) Sugar (mineralocorticoids), Salt (glucocorticoids), and Sex (androgens).
c) Salt (mineralocorticoids), Sugar (glucocorticoids), and Sex (androgens).
d) Salt (glucoocorticoids), Sugar (mineralcorticoids), and Sex (androgens).
13) Anterior pituitary (adenohypophysis) Secretes:

a) FSH, LH, ACTH, prolactin, GH, and β-endorphin.
b) FSH, ACTH, TSH, prolactin, GH, and β-endorphin.
c) FSH, LH, ACTH, TSH, prolactin, GH, and β-endorphin.
d) FSH, LH, ACTH, TSH, prolactin, GH, and β-ectorphin.
14) Melanotropin (MSH) secreted from ____________lobe of pituitary.

a) Anterior
b) Medial
c) Posterior
d) Intermediate
15) Derived from oral ectoderm ( __________ pouch).
a) Monra
b) Lushka
c) Rathke
d) None of above
16) ______subunit—hormone subunit common to _________.

_______ subunit—determines hormone specificity.
a) Alpha and Beta, TSH, LH, FSH, and hCG
b) Alpha and Beta. TSH, FSH and hCG.
c) Beta and Alpha TSH, LH, and hCG
d) Beta and Alpha, TSH, LH, FSH, and hCG
17) Proopiomelanocortin derivatives:

a) β-endorphin, ACTH, and MSH. Go pro with a BAM
b) β-endorphin, ADTH, and MSH. Go pro with a BAM
c) β-ectorphin, ACTH, and MSH. Go pro with a BAM
d) β-endorphin, ADTH, and MSH. Go pro with a BAM
18) FLAT PiG:.

a) FSH, LH, ACTH, TSH, PSL, GH
b) FSH, LH, ACTH, TSH, PRL, GH
c) FSH, LF, ACTH, TSH, PRL, GH
d) FSH, LH, ACTH, TRH, PRL, GH
e)
19) B-FLAT: Basophils—
a) FRH, LH, ACTH, TSH.
b) FSH, LH, ACTH, TRH.
c) FSH, LH, ACTH, TSH.
d) FSH, LH, ACITH, TSH.
20) __________GH, PRL.

a) Basophils:
b) Basosphils:
c) Acidosphils:
d) Acidophils:
21) Posterior pituitary(neurohypophysis): Derived from neuroectoderm

a) Stores and releases vasopressin (antidiuretic hormone, or ADH) and oxytocin, both
made in the thalamus (supraoptic and paraventricular nuclei) and transported to
posterior pituitary via neurophysins (carrier proteins).
b) Stores and releases vasopressin (antidiuretic hormone, or ADH) and oxytocin, both
made in the hypothalamus (supraoptic and paraventricular nuclei) and transported
to posterior pituitary via neurophysins (carrier proteins).
c) Stores and releases vasopressin (antidiuretic hormone, or ADH) and oxytocin, both
made in the hypothalamus (supraoptic and paraventricular nuclei) and transported
to posterior pituitary via neurophysins (proteins).
d) Stores and releases vasopressin (antidiuretic hormone, or ADH) and oxytocin, both
made in the hypothalamus (Infraoptic and paraventricular nuclei) and transported to
posterior pituitary via neurophysins (carrier proteins).
22) Endocrine pancreas cell types Islets of Langerhans are collections of α, β, and δ
endocrine cells. Islets arise from pancreatic buds.
a) α = glucαgon (peripheral), β = insulin (interspersed l), δ = somatostatin (Central)
b) α = glucαgon (Central), β = insulin (Peripheral ), δ = somatostatin (interspersed)
c) α = glucαgon (Peripheral), β = insulin (central), δ = somatostatin (interspersed)
d) α = glucαgon (peripheral), β = insulin (central), δ = somatostatin (interspersed)
23) Preproinsulin (synthesized in _____ of pancreatic ___cells)

a) β cells, RER
b) α cells, SER
c) α cells, RER
d) β cells, SER
24) cleavage of “_____signal ”

a) Postsignal
b) Presignal
c) Both
d) None
25) ___insulin (stored in secretory _______)

a) Pro, Granules
b) Pre, Interganules
c) Pre , Extragranules
d) Pro, No Granules
26) cleavage of_________

a) Proinsulin
b) Insulin
c) Glucagon
d) Glucogen
27) ____________ of insulin and ____-peptide equally.

a) Exocytosis and A-
b) Excocytosis and C-
c) Endocytosis and C
d) Endocytosis and A-
28) Insulin and ___-peptide are __________ in insulinoma and sulfonylurea use, whereas
__genous insulin lacks __-peptide.
a) Decrease, A, Endo
b) Increase, C, Exo
c) Increase, A, Endo
d) Decrease, C,Exo
29) Binds insulin receptors (___________ activity ),

a) pepsine activity
b) tyrosine activity
c) pepsine kinase activity
d) tyrosine kinase activity
30) Binds insulin receptors ________ glucose uptake (carrier mediated transport) into
insulin_____ and ____ transcription
a) Producing, dependent cell, gene
b) Inducing, non-dependent cell, gene
c) Producing, non-dependent tissue, gene
d) Inducing , dependent tissue, gene
31) Anabolic effects of insulin:
A) increase glucose transport in skeletal muscle and adipose tissue, increase glycogen synthesis and
storage, increase triglyceride synthesis, increase Na+ retention (kidneys), increase protein synthesis
(muscles), increase cellular uptake of K+ and amino acids, decrease glucagon release, decrease
lipolysis in adipose tissue
B) increase glucose transport in skeletal muscle and adipose tissue, increase glycogen synthesis and
(muscles), decrease cellular uptake of K+ and amino acids, decrease glucagon release, decrease
C) increase glucose transport in skeletal muscle and adipose tissue, increase glycogen synthesis and
(muscles), increase cellular uptake of K+ and amino acids, increase glucagon release, decrease
D) increase glucose transport in skeletal muscle and adipose tissue, increase glycogen synthesis and
storage, increase triglyceride synthesis, decrease Na+ retention (kidneys), increase protein synthesis
(muscles), increase cellular uptake of K+ and amino acids, decrease glucagon release, decrease
32) _______ glucose, insulin ______ cross placenta.
a. Unlike, does not

b. Like, does not
c. Like, does
d. Unlike, does
33) Insulin-dependent glucose transporters: ƒ GLUT4: adipose tissue, ______ muscle (exercise
can also ______ GLUT4 expression)
a) Striated, decrease
b) Striated, increase
c) Non striated, increase
d) Non striated, decrease
34) Insulin-independent transporters:
A) GLUT1: RBCs, brain, cornea, placenta, GLUT2 (bidirectional): β islet cells, liver, kidney, GI tract
(think 2-way street), GLUT3: brain, placenta, GLUT5 (Fructose): spermatocytes, GI tract,
SGLT1/SGLT2 (Na+-g glucose cotransporters): kidney, Large intestine
B) GLUT1: RBCs, brain, cornea, placenta, GLUT2 (bidirectional): β islet cells, liver, kidney, GI tract
SGLT1/SGLT2 (Na+-g glucose cotransporters): kidney, small intestine
C) GLUT1: RBCs, brain, cornea, placenta, GLUT2 (bidirectional): β islet cells, liver ,kidney, GI tract
D) GLUT1: RBCs, brain, cornea, placenta, GLUT2 (bidirectional): β islet cells, liver ,kidney, GI tract
35) Brain utilizes ________ for metabolism but ketone bodies during starvation.
a) Insulin
b) Glucose
c) Glucagon
d) None
36) RBCs utilize glucose, as they lack _________ for aerobic metabolism
a) mitochondria
b) Nucleus
c) Gogli bodies
d) Lysosome
37) BRICK LIPS (insulin-independent glucose uptake):
a) Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet (α) cells, Placenta, Spermatocytes.
b) Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet cells, Placenta, Spermatocytes.
c) Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet (α -β) cells, Placenta, Spermatocytes.
d) Brain, RBCs, Intestine, Cornea, Kidney, Liver, Islet (β) cells, Placenta, Spermatocytes.
38) Glucose is the major regulator of insulin release. _______insulin response with oral vs IV glucose
due to incretins (eg, glucagon-like peptide 1 [GLP-1], glucose-dependent insulinotropic polypeptide
[GIP]), which are released after meals and ______ β cell sensitivity to glucose.
a) Increase, decrease
b) Increase, increase
c) Decrease, increase
d) Decrease, decrease
39) Release _________ by α2, _______by β2 stimulation (2 = regulates insulin)
a) Increase, decrease
b) Increase, increase
c) Decrease, increase
d) Decrease, decrease
40) Glucose enters β cells:
a) increase ATP generated from glucose metabolism closes K+ channels (target of sulfonylureas) and
depolarizes β cell membrane Voltage-gated Ca2+ channels open Ca2+ influx and stimulation of
insulin exocytosis .
b) increase ATP generated from glucose metabolism closes K+ channels (target of sulfonylureas) and
depolarizes β cell membrane Voltage-gated Ca2+ channels open Ca2+ influx and stimulation of
insulin endocytosis .
a) decrease ATP generated from glucose metabolism closes K+ channels (target of sulfonylureas)
and depolarizes β cell membrane Voltage-gated Ca2+ channels open Ca2+ influx and stimulation of
a) decrease ATP generated from glucose metabolism closes K+ channels (target of sulfonylureas)
and depolarizes β cell membrane Voltage-gated Ca2+ channels open Ca2+ influx and stimulation of
41) Glucagon SOURCE Made by ____cells of _______.
a) α cells, liver
b) β cells, pancreas
c) β cells, liver
d) α cells, pancreas
42) _________ glycogenolysis, gluconeogenesis, lipolysis, ketogenesis.
a) Promotes
b) Induce
c) Reduce
d) Increase
43) Elevates blood sugar levels to maintain homeostasis when bloodstream glucose levels fall too
_________ (ie, fasting state).
a) High
b) Low
c) both
d) None
44) _________in response to hypoglycemia.
a) Control
b) Secreted
c) Reduce
d) Increase
45) ___________ by insulin, hyperglycemia, and somatostatin.
a) Excited
b) Inhibited
c) Secreted
d) Control
46) ADH __________ water permeability of distal convoluted tubule and collecting duct cells in
kidney to __________ water reabsorption.
a) a) Increase, decrease
b) b) Increase, increase
c) c) Decrease, increase
d) d) Decrease, decrease
47) Stimulus for secretion is _____________plasma osmolality, except in SIADH, in which ADH is
elevated despite __________ plasma osmolality.
48) CRH __________ ACTH, MSH, β-endorphin ____________ in chronic exogenous steroid use.
49) Dopamine decrese prolactin, TSH Also called ________________.
a) prolactin-inhibiting factor.
b) prolactin-excitory factor.
c) CRH-inhibiting factor.
d) Insulin-inhibiting factor.
50) Dopamine antagonists (eg, antipsychotics) can cause galactorrhea due to ___________
a) Hypoprolactinemia
b) Hyperprolactinemia
c) Hyperprelactinemia
d) Hyperproslactinemia
51) GHRH ____________GH Analog (tesamorelin) used to treat HIV-associated lipodystrophy.
a) Increase,
b) decrease
c) Reduce
d) None
52) GnRH ____________ FSH, LH Suppressed by hyperprolactinemia.
a) Increase,
b) decrease
c) Reduce
d) None
53) Tonic GnRH ___________ HPG axis.
a) Induce
b) Reduce
c) Suppresses
d) Control
54) Pulsatile ______leads to puberty, fertility
a) GnRH
b) GHRH
c) CRH
d) ADH
55) MSH _________ melanogenesis by melanocytes Causes hyperpigmentation in Cushing disease,

as MSH and ACTH share the same precursor molecule, proopiomelanocortin.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
56) __________ Causes uterine contractions during labor.
a) Prolactin
b) Oxytocin
c) Insulin
d) Proinsulin
57) Responsible for milk let down ________ in response to suckling. Modulates fear, anxiety, social
bonding, mood, and depression.
a) Reflex
b) voluntary
c) none
d) involuntary
58) Analogs used to induce labor, strengthen uterine contractions and control postpartum
_______
a) hemolysis
b)hemorrhage.
c) hemiplegia
d) none
59) __________ GnRH Pituitary prolactinoma -> amenorrhea, osteoporosis, hypogonadism,

galactorrhea.
a) Prolactin
b) Oxytocin
c) Insulin
d) Proinsulin
60) Breastfeeding ________ prolactin _________ GnRH delayed postpartum ovulation (natural
contraception).
61) Somatostatin ____________ GH, TSH Analogs used to treat acromegaly

a) Increase,
b) decrease
c) Reduce
d) None
62) TRH _________TSH, prolactin ____________TRH (eg, in 1°/2° hypothyroidism) may increase
prolactin secretion galactorrhea.
63) Prolactin SOURCE Secreted mainly by ________pituitary. Structurally _____________to growth

hormone
a) anterior, homologous
b) anterior heterologous
c) Posterior heterologous
d) Posterior homologous
64) Stimulates milk production in breast; inhibits ovulation in females and spermatogenesis
in males by inhibiting GnRH synthesis and release.
a) Prolactin
b) Oxytocin
c) Insulin
d) Proinsulin
65) Excessive amounts of prolactin associated with _________ libido.
a) Increase,
b) decrease
c) Reduce
d) None
66) Prolactin secretion from anterior pituitary is tonically inhibited by dopamine from
tuberoinfundibular pathway of _______________.
a) cerebellum
b) Basal ganglia
c) thalamus.
d) hypothalamus.
67) Prolactin in turn inhibits its own secretion by increase dopamine synthesis and secretion
from _______________.
a) cerebellum
b) Basal ganglia
c) thalamus.
d) hypothalamus.
68) TRH __________ prolactin secretion (eg, in 1° or 2° hypothyroidism).
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) None
69) ____________ agonists (eg, bromocriptine) inhibit prolactin secretion and can be used in
treatment of prolactinoma.
a) GnRH
b) GHRH
c) CRH
d) Dopamine
70) ___________ antagonists (eg, most antipsychotics) and estrogens (eg, OCPs, pregnancy)
stimulate prolactin secretion.
a) GnRH
b) GHRH
c) CRH
d) Dopamine
71) Growth hormone Also called ______________.
a) mesototropin
b)exototropin
c) somatotropin
d) endototropin
72) GH Secreted by ________ pituitary.
a) posterior
b) anterior
c) both
d) none
73) GH Stimulates linear growth and muscle mass through IGF-1 (somatomedin C) secretion by
a) kidney
b) gall bladder
c) liver.
d) spleen
74) GH ______insulin resistance (diabetogenic)

a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) None
75) GH Released in pulses in response to growth hormone–___________hormone (GHRH).
a) Inhibiting
b) Releasing
c) Excitating
d) Control
76) Released in pulses in response to growth hormone ________ hormone (GHRH).
a) Inhibiting
b) Releasing
c) Excitating
d) Control
77) GH Secretion inhibited by glucose, somatostatin, and somatomedin
(regulatory molecule secreted by ______ in response to GH acting on target tissues).
a) Liver
b) Kidney
c) Gall bladder
d) Spleen
78) Excess secretion of _______(eg, pituitary adenoma) may cause acromegaly (adults) or gigantism
(children). Treat with somatostatin analogs (eg,octreotide) or surgery.
a) GHRH
b) GnRH
c) GH
d) ADH
79) Stimulates hunger (orexigenic effect) and GH release (via GH secretagogue receptor).
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
80) Appetite regulation
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
81) Sleep deprivation or Prader-Willi syndrome increase ___________ production.
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
82) ___________makes you hunghre and ghrow
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
83) ___________ Acts on lateral area of hypothalamus (hunger center) to increase appetite.
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
84) Leptin Satiety hormone. Produced by adipose tissue. Mutation of leptin gene congenital obesity.
Sleep deprivation or starvation _________leptin production.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) None
85) Leptin keeps you ______. Acts on ventromedial area of ________ (satiety center) to
________appetite.
a) thin, thalamus, increase
b) thick, thalamus, decrease
c) thin, hypothalamus, decrease
d) thick, hypothalamus, increase
86) ____________Act at cannabinoid receptors in __________ and nucleus accumbens, two key
brain areas for the homeostatic and hedonic control of food intake increase appetite.
a) Ghrelin, thalamus
b) Leptin, hypothalamus
c) Endocannabinoids, hypothalamus
d) All
87) Exogenous cannabinoids cause “the munchies.”
a) Ghrelin
b) Leptin
c) Endocannabinoids
d) All
88) _______hormone Also called vasopressin.
a) ADH
b) GH
c) GnRH
d) None
89) ____________SOURCE Synthesized in hypothalamus (supraoptic and
paraventricular nuclei), stored and secreted by ____________ pituitary.
a) ADH, posterior
b) GH, anterior
c) GnRH, posterior
d) None
90) Regulates serum osmolality (V2-receptors) and blood pressure (V1-receptors).
a) ADH
b) GH
c) GnRH
d) None
91) Primary function is serum osmolality regulation (ADH _____serum osmolality, _____ urine
osmolality) via regulation of aquaporin channel insertion in principal cells of renal collecting duct.
92) ADH level is _______ in central diabetes insipidus (DI), normal or _______ in nephrogenic DI.
93) Nephrogenic DI can be caused by mutation in _______-receptor.
a) V1
b) V2
c) V3
d) V4
94) -----------(ADH analog) is a treatment for central DI and nocturnal enuresis
a) Desmopressin
b) Nephrogenic
c) Vasopressin
d) None
95) All congenital adrenal enzyme deficiencies are autosomal recessive disorders and most are
characterized by skin hyperpigmentation (due to ________MSH production, which is coproduced
and secreted with ACTH) and bilateral adrenal gland enlargement (due to ______ ACTH stimulation).
96) If deficient enzyme starts with 1, it causes_____________; if deficient enzyme ends with 1, it
causes virilization in females
a) Hypertension
b) none
c)tension
d)hyportension
97) Cortisol SOURCE Adrenal zona fasciculata. Bound to corticosteroid-________ globulin
a) binding
b) inhibiting
c) excitation
d) control
98) ________ Appetite _________Blood pressure: Upregulates α1-receptors on arterioles

________sensitivity to norepinephrine and epinephrine (permissive action)
a) a) Increase, decrease, increase
b) b) Increase, increase, increase
c) c) Decrease, increase, decrease
d) d) Decrease, decrease, decrease
99) At __________ concentrations, can bind to mineralocorticoid (aldosterone) receptors
a) high
b) low
c) control
d) none
100) _______ Insulin resistance (diabetogenic)
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
101) ___________Gluconeogenesis, lipolysis, and proteolysis (_________glucose utilization)
102) _________ Fibroblast activity (poor wound healing,_______collagen synthesis, ______ striae)
a) a) Increase, decrease, increase
b) b) Increase, increase, increase
c) c) Decrease, decrease, increase
d) d) Decrease, decrease, decrease
103) decrease Inflammatory and Immune responses:

a) Inhibits production of leukotrienes andprostaglandins. Inhibits WBC adhesion neutrophilia. Blocks
histamine release from mast cells. Eosinopenia, lymphopenia. Blocks IL-2 production
b) excitated production of leukotrienes andprostaglandins. Inhibits WBC adhesion neutrophilia.

Blocks histamine release from mast cells. Eosinopenia, lymphopenia. Blocks IL-2 production
c) Increase production of leukotrienes andprostaglandins. Inhibits WBC adhesion neutrophilia.

d) decrease production of leukotrienes andprostaglandins. Inhibits WBC adhesion neutrophilia.

104) ________Bone formation (___________osteoblast activity)
105) Cortisol is A BIG FIB. _________ corticosteroids can cause reactivation of TB and candidiasis
(blocks IL-2 production).
a) Endogeneous
b) Exogenous
c) Mesogenous
d) none
106) REGULATION CRH (hypothalamus) stimulates ACTH _________ (pituitary) cortisol production in
adrenal zona fasciculata.
a) Produce
b) Release
c) Control
d) none
107)Excess cortisol _________ CRH, ACTH, and cortisol secretion. Chronic stress _________
prolonged secretion
a) a) Increase, reduce
b) b) decrease, induce
c) c) Reduce, decrease
d) d) Suppress, increase
108) Calcium homeostasis Plasma Ca2+ exists in three forms:

a) ƒ Ionized/free (~ 40%, active form) ƒ Bound to albumin (∼ 40%) Bound to anions (∼ 15%)
b) Ionized/free (~ 45%, active form) Bound to albumin (∼ 40%) Bound to anions (∼ 15%)
c) Ionized/free (~ 45%, active form) Bound to albumin (∼ 30%) Bound to anions (∼ 13%)
d) Ionized/free (~ 45%, active form) Bound to albumin (∼ 40%) Bound to anions (∼ 15%)
109) Ca homeostasis _______ pH (less H+) albumin binds more Ca2+ _______ionized Ca2+
(eg, cramps, pain, paresthesias, carpopedal spasm) ______ PTH. _____ pH (more H+) _____
albumin binds less Ca2+ ________ ionized Ca2+  PTH.
a) a) Increase, decrease, increase, decrease, increase, decrease
b) b) Increase, increase, increase decrease, increase, decrease
c) c) Decrease, decrease, increase decrease, increase, decrease
d) d) Decrease, decrease, decrease decrease, increase, decrease
110) _______________Ionized/free Ca2+ is 1° regulator of PTH; changes in pH alter PTH

secretion, whereas changes in albumin concentration do not.
a) cortisol
b) Calcium homeostasis
c) Albumin
d) Calcium
111) Chief cells of parathyroid. FUNCTION _____bone resorption of Ca2+ and PO4 3−.
_____kidney reabsorption of Ca2+ in distal convoluted tubule.
112) __________ reabsorption of PO43− in proximal convoluted tubule.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
113) ________1,25-(OH)2 D3 (calcitriol) production by stimulating kidney 1α-hydroxylase in

proximal convoluted tubule
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
114) PTH ____ serum Ca2+, ______serum PO43–, _____ urine PO43– , ____urine cAMP.
a) a) Increase, decrease, increase,increase
b) b) Increase, increase, increase,increase
c) c) Decrease, decrease, increase,decrease
d) d) Decrease, decrease, decrease, decease
115) RANK-L (receptor activator of NF-κB ligand) secreted by _________________
a) osteoblasts
b) osteocytes
c) both
d) none
116) Binds RANK (receptor) on osteoclasts and their precursors to stimulate osteoclasts and
__________ Ca2+,bone resorption.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
117)Intermittent PTH_________________ can also stimulate bone formation.
a) Produce
b) Release
c) Control
d) none
118) PTH = Phosphate-Trashing Hormone. PTH-related peptide (PTHrP) functions like PTH
and is commonly _______________ in malignancies (eg, squamous cell carcinoma of the
lung, renal cell carcinoma)
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
119) _________ serum Ca2+ ___________ PTH secretion.
120) ______________ serum PO4 3− _________ PTH secretion. ___________ serum Mg2+ ________
PTH secretion. __________serum Mg2+ __________PTH secretion.
a) a) Increase, decrease, increase, increase, increase, decrease, increase, decrease,

increase
b) b) Increase, increase, increase, increase, increase, decrease, increase, decrease,

increase
c) c) Decrease, decrease, increase, decrease, increase, decrease, increase, decrease,

increase
d) d) Decrease, increase, increase, increase, decrease, increase, decrease, decrease,

decrease
121)Common causes of ______Mg2+ include diarrhea, aminoglycosides, diuretics, alcohol abuse.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
122) Calcitonin SOURCE Parafollicular cells (____cells) of thyroid
a) A
b) B
c) C
d) D
123) Calcitonin opposes actions of _______. Not important in normal Ca2+ homeostasis.
Calcitonin tones down serum Ca2+ levels and keeps it in bones.
a) PH
b) PTH
c) GH
d) Calcitonin
124) Calcitonin FUNCTION __________ bone resorption of Ca2+. REGULATION ________ serum Ca2+
calcitonin secretion.
125) _____________ Iodine-containing hormones that control the body’s metabolic rate.
a) Thyroid hormones (T2/T3)
b) Thyroid hormones (T2/T4)
c) Thyroid hormones (T2/T3)
d)Thyroid hormones (T3/T4)
126) Follicles of thyroid. 5′-deiodinase converts _____________________________(5, 4, 3).
a) T4 (the major thyroid product) to T3 in peripheral tissue
b) T3(the major thyroid product) to T2 in peripheral tissue
c) T2 (the major thyroid product) to T4 in peripheral tissue
d) T2 (the major thyroid product) to T3 in peripheral tissue
127) Peripheral conversion is_________ by glucocorticoids, β-blockers and propylthiouracil (PTU).
a) binding
b) excitted
c) inhibited
d) release
128) Functions of thyroid peroxidase include oxidation, organification of iodide and coupling of
monoiodotyrosine (MIT) and diiodotyrosine (DIT). ___________by PTU and methimazole. DIT +
DIT = T4. DIT + MIT = T3. Wolff-Chaikoff effect—excess iodine temporarily turns off thyroid
peroxidase decrease T3/T4 production (protective autoregulatory effect).
a) binding
b) excitted
c) inhibited
d) release
129) Only free hormone is active. T___ binds nuclear receptor with greater affinity than T___. T__
functions.
a) a) Thyroid hormones (T2/T3)

b) b) Thyroid hormones (T2/T4)
c) c) Thyroid hormones (T2/T3)
d) d)Thyroid hormones (T3/T4)
130) —6 B’s: a) ƒ Brain maturation, Bone growth (synergism with GH), β-adrenergic effects. ____ β1
receptors in heart ____ CO, HR, SV, contractility; β-blockers alleviate adrenergic symptoms in
thyrotoxicosis
Basal metabolic rate ________(via Na+/K+-ATPase activity _______O2 consumption, RR, body
temperature) ƒ Blood sugar (_______glycogenolysis, gluconeogenesis) ƒ Break down lipids
(______lipolysis
a) a) Increase, decrease, increase,increase, increase, increase
b) b) Increase, increase, increase, Increase, increase, increase
c) c) Decrease, decrease, increase , decrease, increase, decrease
d) d) Decrease, decrease, decrease, decease, decrease, decrease
131) TRH ⊕ TSH release ⊕ follicular cells. Thyroid-___________ immunoglobulin (TSI) may
follicular cells in Graves disease.
a) Releasing
b) Stimulating
c) Inhibiting
d) excitating
132) Negative feedback primarily by free T3/T4:
a) Anterior pituitary decrease sensitivity to TRH Hypothalamus decrease TRH secretion
b) posterior pituitary decrease sensitivity to TRH Hypothalamus decrease TRH secretion
c) Anterior pituitary increase sensitivity to TRH Hypothalamus increase TRH secretion
d) posterior pituitary increase sensitivity to TRH Hypothalamus increase TRH secretion
133)Thyroxine-binding globulin (TBG) binds most T3/T4 in blood. Bound T3/T4 = inactive.
______TBG in pregnancy, OCP use (estrogen ___________ TBG) _________ total T3/T4
_______________ TBG in hepatic failure, steroid use, nephrotic syndrome
b) b) Increase, increase, increase, decrease
134) cAMP:
a) FSH, LH, ACTH, TSH, CRH, hCG, ADH (V1-receptor), MSH, PTH, calcitonin, GHRH,
glucagon, histamine (H1-receptor).
b) FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2-receptor), MSH, PTH, calcitonin, GHRH,
c) FSH, LH, ACTH, TSH, CRH, hCG, ADH (V3-receptor), MSH, PTH, calcitonin, GHRH,
d) FSH, LH, ACTH, TSH, CRH, hCG, ADH (V4-receptor), MSH, PTH, calcitonin, GHRH,
135) cGMP
a) BNP, ANP, EDRF (NO) BAD GraMPa Think vasodilators
b) BNP, ANP, EDRF (NO) BAD GraMPa Think vasocontriction
c) BNP, ANP, ERF (NO) BAD GraMPa Think vasodilators
d) BNP, ANP, EDF (NO) BAD GraMPa Think vasodilators
136) ________GnRH, Oxytocin, ADH (V1-receptor), TRH,Histamine (H1-receptor), Angiotensin II,
Gastrin GOAT HAG
a) IP4
b) IP3
c) IP2
d) IP1
137) ___________ receptor Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, T3/T4,

Vitamin D PET CAT on TV
a) cellular
b) Intercellular
c) Extracellular
d) Intracellular
138) Receptor_________________, IGF-1, FGF, PDGF, EGF MAP kinase pathway Think Growth
Factors (Get Found In the MAP)
a) kinase Insulin
b) prosine kinase Insulin
c) tyrosine Insulin
d) tyrosine kinase Insulin
139) Nonreceptor __________ Prolactin, Immunomodulators (eg, cytokines IL-2, IL-6, IFN), GH, G-
CSF, Erythropoietin, Thrombopoietin JAK/STAT pathway Think acidophils and cytokines PIGGLET
Factors (Get Found In the MAP)
a) kinase
b) prosine kinase
c) tyrosine
d) tyrosine kinase
140) Steroid hormones are lipophilic and therefore must circulate bound to specific binding
globulins, which ________their solubility.In men, ________sex hormone–binding globulin (SHBG)
lowers free testosterone gynecomastia. In women, _______SHBG raises free testosterone
hirsutism. OCPs, pregnancy _________ SHBG.
b) b) Increase, increase, decrease, increase
141) Cushing syndrome ETIOLOGY ______ cortisol due to a variety of causes:
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
142) Exogenous corticosteroids _______ ACTH bilateral adrenal atrophy.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
143) Primary adrenal adenoma, hyperplasia, or carcinoma—results in ________ ACTH atrophy of
uninvolved adrenal gland.
a) a) Increase,
b) b) decrease
c) c) Reduce
d) d) Suppress
144) ƒ ACTH-secreting pituitary adenoma (Cushing disease);
a)paraneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids) bilateral adrenal
hyperplasia.
b) preneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids) bilateral adrenal
hyperplasia.
c) paraneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids) bilateral adrenal
hypoplasia.
d) preneoplastic ACTH secretion (eg, small cell lung cancer, bronchial carcinoids) bilateral adrenal
hyporplasia.
145) Cushing disease is responsible for the majority of _________cases of Cushing syndrome.
a) endogenous
b) exogenous
c) both
d) none
146) Cushing disease:
a) Hypotension, weight gain, moon facies A , truncal obesity, buffalo hump, skin changes (eg,
thinning, striae B ), hirsutism, osteoporosis, hyperglycemia (insulin resistance), amenorrhea,
immunosuppression. Can also present with pseudohyperaldosteronism.
b)Hypertension, weight gain, moon facies A , truncal obesity, buffalo hump, skin changes (eg,
thinning, striae B ), hirsutism, osteoporosis, hypoglycemia (insulin resistance), amenorrhea,
c)Hypertension, weight gain, moon facies A , truncal obesity, buffalo hump, skin changes (eg,
thinning, striae B ), hirsutism, osteoporosis, hyperglycemia (insulin resistance), demnorrhea,
d) Hypertension, weight gain, moon facies A , truncal obesity, buffalo hump, skin changes (eg,
thinning, striae B ), hirsutism, osteoporosis, hyperglycemia (insulin resistance), amenorrhea,
147) Cushing Disease Screening tests include: ___________ free cortisol on 24-hr urinalysis,
__________ late night salivary cortisol, and no suppression with overnight low-dose dexamethasone
test
148) Nelson syndrome
a) Removal of cortisol feedback mechanism after bilateral adrenalectomy for refractory Cushing
disease enlargement of existing ACTH-secreting pituitary adenoma. Presents with
hypopigmentation, headaches, bitemporal hemianopia.
b) Removal of cortisol feedback mechanism after bilateral adrenalectomy for refractory Cushing
disease enlargement of existing PCTH-secreting pituitary adenoma. Presents with
hyperpigmentation, headaches, bitemporal hemianopia
c) Removal of cortisol feedback mechanism after bilateral adrenalectomy for refractory Cushing
disease enlargement of existing ACTH-secreting pituitary adenoma. Presents with
hyperpigmentation, headaches, bitemporal hemianopia.
d) Removal of cortisol feedback mechanism after bilateral adrenalectomy for refractory Cushing
disease enlargement of existing ACTH-secreting pituitary adenoma. absent with hyperpigmentation,
headaches, bitemporal hemianopia.
149) Treatment: pituitary irradiation or surgical resection.
a) Cushing disease
b) Nelson syndrome
c) Adrenal insufficie y
d) Hyperaldosteronism
150) Inability of adrenal glands to generate enough glucocorticoids +/− mineralocorticoids for the
body’sneeds. Symptoms include weakness, fatigue, orthostatic hypotension, muscle aches, weight
loss, GI disturbances, sugar and/or salt cravings. Treatment: glucocorticoid/mineralocorticoid
replacement.
a) Cushing disease
b) Nelson syndrome
c) Adrenal insufficie y
d) Hyperaldosteronism
151) Deficiency of aldosterone and cortisol production due to loss of gland function hypotension
(hyponatremic volume contraction), hyperkalemia, metabolic acidosis, skin/mucosal
hyperpigmentation A (increase melanin synthesis due to increase MSH, a byproduct of ACTH
production from POMC).
a) Primary adrenal insufficiency
b) Secondary adrenal insufficiency
c) Tertiary adrenal insufficiency
d) none
152) Acute—sudden onset (eg, due to massive hemorrhage). May present with shock in
acute adrenal crisis.
d) none
153) ƒ Chronic—__________. Due to adrenal atrophy or destruction by disease (autoimmune

destruction most common in the Western world; TB most common in the developing world).
a) autoimmune glandular syndromes.
b) autoimmune polyglandular syndromes.
c) Waterhouse-Friderichsen syndrome
d) Addison disease
154) Primary Pigments the skin/mucosa. Associated with _________________.
d) Addison disease
155)_________________—acute 1° adrenal insufficiency due to adrenal
hemorrhage associated with septicemia(usually Neisseria meningitidis), DIC,endotoxic shock.
d) Addison disease
156) Seen with pituitary ACTH production. No skin/mucosal hyperpigmentation (ACTH is
not elevated), no hyperkalemia (aldosterone synthesis preserved due to functioning adrenal
gland, intact RAAS).
d) none
157) ____________ Spares the skin/mucosa.
a) primary
b) secondary
c) tertiary
d) none
158) Seen in patients with chronic exogenous steroid use, precipitated by abrupt withdrawal.
Aldosterone synthesis unaffected.

d) none
159) Hyperaldosteronism _____________ secretion of aldosterone from adrenal gland
a) a) Increased
b) b) decreased
c) c) Reduce
d) d) Suppress
160) Clinical features include hypertension,_________ or normal K+, metabolic alkalosis. 1°

hyperaldosteronism does not directly cause edema due to aldosterone escape mechanism.
However, certain 2° causes of hyperaldosteronism (eg, heart failure) impair the aldosterone escape
mechanism, leading to worsening of edema.
a) a) Increased
b) b) decreased
c) c) Reduce
d) d) Suppress
161) Seen with adrenal adenoma (Conn syndrome) or bilateral adrenal hyperplasia. increase
aldosterone, decrease renin. Leads to treatment-resistant hypertension.
a) Primary hyperaldosteronism
b) Secondary hyperaldosteronism
c) Tertiary hyperaldosteronism
d) none
162) Seen in patients with renovascular hypertension, juxtaglomerular cell tumors (renin-producing),
and edema (eg, cirrhosis, heart failure, nephrotic syndrome).
a) Primary hyperaldosteronism
b) Secondary hyperaldosteronism
c) Tertiary hyperaldosteronism
d) none
163) Neuroendocrine tumors
a) Heterogeneous group of neoplasms originating from neuroendocrine cells (which has traits similar
to nerve cells and hormone-producing cells).
b) Homogeneous group of neoplasms originating from neuroendocrine cells (which has traits similar

c)Heterogeneous group of neoplasms originating from neuroexocrine cells (which has traits similar
d)Heterogeneous group of neoplasms originating from neuroendocrine cells (which has traits
different to nerve cells and hormone-producing cells).
164) Neuroendocrine tumors
a) Most neoplasms occur in the GI system (eg, carcinoid, gastrinoma), pancreas (eg, insulinoma,
glucagonoma), and lungs (eg, small cell carcinoma). Also in thyroid (eg, medullary carcinoma) and
adrenals (eg, pheochromocytoma).
b) Most neoplasms decrease in the GI system (eg, carcinoid, gastrinoma), pancreas (eg, insulinoma,
c) Most neoplasms increase in the GI system (eg, carcinoid, gastrinoma), pancreas (eg, insulinoma,
d) Most neoplasms occur in the GI system (eg, carcinoid, gastrinoma), pancreas (eg, insulinoma,
glucagonoma), and lungs (eg, small cell carcinoma). Also in thyroid (eg, cortex carcinoma) and
165) Neuroendocrine tumors:
a) Characteristics differ depending on anatomical site, cell(s) of origin (eg, enterochromaffin cells,
enterochromaffin-like cells, pancreatic β cells), and secretory products (eg, chromogranin A, neuron-
specific enolase [NSE], serotonin, histamine, calcitonin). Cells contain amine precursor uptake
decarboxylase (APUD).
b) Characteristics differ depending on anatomical site, cell(s) of origin (eg, enterochromaffin cells,
enterochromaffin-like cells, pancreatic β cells), and secretory products (eg, chromogranin B, neuron-
c) Characteristics differ depending on anatomical site, cell(s) of origin (eg, enterochromaffin cells,
enterochromaffin-like cells, pancreatic β cells), and secretory products (eg, chromogranin C, neuron-
d) Characteristics differ depending on anatomical site, cell(s) of origin (eg, enterochromaffin cells,
enterochromaffin-like cells, pancreatic β cells), and secretory products (eg, chromogranin D, neuron-
166) Neuroblastoma
a) Most common tumor of the adrenal medulla A in children, usually < 4 years old. Originates from
Neural crest cells. Occurs anywhere along the sympathetic chain.
b) Most common presentation is abdominal distension and a firm, irregular mass that can cross the
midline (vs Wilms tumor, which is smooth and unilateral). Less likely to develop hypertension
than with pheochromocytoma (Neuroblastoma is Normotensive).
c)Can also present with opsoclonus-myoclonus syndrome (“dancing eyes-dancing feet”).
HVA and VMA (catecholamine metabolites) in urine.
d)Homer-Wright rosettes B characteristic of neuroblastoma and medulloblastoma. Bombesin and

NSE ⊕. Associated with amplification of N-myc oncogene. Classified as an APUD tumor.
RBCs
1) Anemia of chronic disease
a) Inflammation (eg, decrease IL-6) decrease hepcidin (released by liver, binds ferroportin on
intestinal mucosal cells and macrophages, thus inhibiting iron transport) decrease release of
iron from macrophages and increase iron absorption from gut.
b) Associated with conditions such as chronic infections, neoplastic disorders, chronic kidney
disease, and autoimmune diseases (eg, SLE, rheumatoid arthritis). increase iron, increase
TIBC, increase ferritin.
c) Normocytic, but can become macrocytic.
d) Treatment: address underlying cause of inflammation, judicious use of blood transfusion,
consider erythropoiesis inhibiting agents such as EPO (eg, in chronic kidney disease).
2) Aplastic anemia
a) A Caused by failure or destruction of hematopoietic stem cells due to: ƒ Radiation and
drugs (eg, benzene, chloramphenicol, alkylating agents, antimetabolites) ƒ Viral agents
(EBV, HIV, hepatitis viruses) ƒ Fanconi anemia (DNA repair defect causing liver failure;
normocytosis or macrocytosis may be seen on CBC); also short stature, incidence of
tumors/ leukemia, café-au-lait spots, thumb/radial defects ƒ Idiopathic (immune
mediated, 2° stem cell defect); may follow chronic hepatitis. reticulocyte count,
EPO.
b) Pancytopenia characterized by hypoanemia, leukopenia, and thrombocytopenia (not to
be confused with aplastic crisis, which causes anemia only). Normal cell morphology, but
hypercellular bone marrow with fatty infiltration A (dry bone marrow tap).
c) Symptoms: fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
d) Treatment: withdrawal of offending agent, immunoproduce regimens (eg,
antithymocyte globulin, cyclosporine), bone marrow allograft, RBC/platelet transfusion,
bone marrow inhibition (eg, GM-CSF).
3) Hereditary spherocytosis
a) Intravascular hemolysis due to defect in proteins interacting with RBC membrane
skeleton and plasma membrane (eg, ankyrin, band 3, protein 4.3, spectrin).
b) Mostly autosomal dominant inheritance. Results in small, round RBCs with more surface
area and central pallor ( MCHC) premature removal by spleen.
c) Splenomegaly, aplastic crisis (parvovirus B16 infection).
d) Labs: mean fluorescence of RBCs in eosin 5-maleimide (EMA) binding test, fragility
in osmotic fragility test. Normal to MCV with abundance of RBCs. Treatment:
splenectomy.
4) G6PD deficiency
a) Defect in G6PD increase NADPH increase reduced glutathione decrease RBC
susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans)
hemolysis.
b) Causes extravascular and intravascular hemolysis. Y-linked recessive.
c) Back pain, hemoglobinuria a few days after oxidant stress.
d) Labs: blood smear shows RBCs with Heinz bodies and Red cells.
5) Pyruvate kinase deficiency
a) Autosomal dominant
b) Pyruvate kinase defect decrease ATP rigid RBCs extravascular hemolysis.
c) decrease levels of 2,3-BPG hemoglobin affinity for O2.
d) Hemolytic anemia in a adult.
6) Paroxysmal nocturnal hemoglobinuria
a) Increase complement-mediated intravascular RBC lysis (acquired mutation in PIGA gene
impaired synthesis of GPI anchor for decay-accelerating factor [DAF/CD55] and
membrane inhibitor of reactive lysis [MIRL/CD59] that protects RBC membrane from
complement).
b) Acquired mutation in a hematopoietic stem cell. Decrease incidence of acute leukemias.
Associated with aplastic anemia.
c) Triad: Coombs ⊝ hemolytic anemia, hypopancytopenia, venous thrombosis (eg,
BuddChiari syndrome). Patients may report yellow or pink urine.
d) Labs: CD55/56 ⊝ RBCs on flow hypercytometry. Treatment: eculizumab (targrgets
terminal complement protein C6).
7) Sickle cell anemia
a) HbS point mutation causes a many amino acid replacement in alpha chain (substitution
of glutamic acid with valine). Causes extravascular and intravascular hemolysis.
b) Pathogenesis: high O2, low altitude, or acidosis precipitates sickling (oxygenated HbS
polymerizes) anemia, vaso-occlusive disease. Newborns are initially asymptomatic
because of decrease HbF and increase HbS. Homoozygotes (sickle cell trait) have
resistance to malaria. 8% of African Americans carry an HbS allele. Sickle cells are
crescent-shaped RBCs A . “Crew cut” on skull x-ray due to marrow expansion from
erythropoiesis (also seen in thalassemias).
c) Complications in sickle cell disease: ƒ Aplastic crisis (transient arrest of erythropoiesis
due to parvovirus B19). ƒ Autosplenectomy (Howell-Jolly bodies) risk of infection by
encapsulated organisms (eg, S pneumoniae). ƒ Splenic infarct/sequestration crisis. ƒ
Salmonella osteomyelitis. ƒ Painful vaso-occlusive crises: dactylitis (painful swelling of
hands/feet), priapism, acute chest syndrome (respiratory distress, new pulmonary
infiltrates on CXR, common cause of death), avascular necrosis, stroke. ƒ Sickling in renal
medulla ( Po2) renal papillary necrosis hematuria.
d) Diagnosis: hemoglobin electrophoresis. Treatment: hydroxyurea (decrease HbF),
hydration.
8) HbC disease
a) Glutamic acid–to-lyCine (lysine) mutation in alpha-globin.
b) Causes intravascular hemolysis.
c) Patients with HbSC (1 of each mutant gene) have milder disease than HbSS patients.
d) Blood smear in heterozygotes: hemoglobin Crystals inside RBCs, target cells.
9) Autoimmune hemolytic anemia

a) A Warm (IgM)—acute anemia seen in SLE and CLL and with certain drugs (eg, beta-
methyldopa) (“warm weather is Great”).
b) Cold (IgG and complement)—chronic anemia triggered by cold; seen in CLL, Mycoplasma
pneumoniae infections, and infectious Multinucleosis (“cold weather is MMMiserable).
c) RBC agglutinates A may cause painful, blue fingers and toes with cold exposure. Many
warm and cold AIHAs are idiopathic. Autoimmune hemolytic anemias are usually
Coombs ⊕.
d) Direct Coombs test— normal RBCs added to patient’s serum. If serum has anti-RBC
surface Ig, RBCs agglutinate when Coombs reagent added Indirect Coombs test—. anti-Ig
antibody (Coombs reagent) added to patient’s RBCs. RBCs agglutinate if RBCs are coated
with Ig
10) Microangiopathic anemia
a) Pathogenesis: RBCs are damaged when passing through obstructed or narrowed vessel
lumina.
b) Seen in DIC, TTP/HUS, SLE, HELLP syndrome, hypotensive emergency.
c) Schistocytes (eg, “helmet cells”) are not seen on peripheral blood smear due to
chemical destruction (schisto = to split) of RBCs.
d) NONE
11) Macroangiopathic anemia
a) Prosthetic heart valves and aortic stenosis may also cause hemolytic anemia 1° to
mechanical destruction of RBCs. Schistocytes on peripheral blood smear.
b) Prosthetic heart valves and aortic stenosis may also cause hemolytic anemia 2° to
c) Prosthetic heart valves and aortic stenosis may also cause hemolytic anemia 3° to
d) Prosthetic heart valves and aortic stenosis may also cause hemolytic anemia 4° to
12) Infections
a) Increase destruction of RBCs (eg, malaria, Babesia).
b) decrease destruction of RBCs (eg, malaria, Babesia).
c) destruction of RBCs (eg, malaria, Babesia).
d) None
13) Interpretation of iron studies
a) increase-decreae = 1° disturbance. Transferrin—transports iron in blood. TIBC—indirectly

measures transferrin. Ferritin—1° iron storage protein of body. aEvolutionary reasoning—pathogens
use circulating iron to thrive. The body has adapted a system in which iron is stored within the cells
of the body and prevents pathogens from acquiring circulating iron.
b) decreae-increase = 2° disturbance. Transferrin—transports iron in blood. TIBC—indirectly

c)) increase-increase = 3° disturbance. Transferrin—transports iron in blood. TIBC—indirectly
d) decrease-decrease = 4° disturbance. Transferrin—transports iron in blood. TIBC—indirectly

14) Neutropenia
a) Absolute neutrophil count < 1300 cells/mm3 acute infections typical when < 500 cells/mm3
Sepsis/postinfection, drugs (including chemotherapy), aplastic anemia, SLE, radiation
b) Absolute neutrophil count > 1500 cells/mm3 Severe infections typical when < 400 cells/mm3
c) Absolute neutrophil count < 1500 cells/mm3 Severe infections typical when < 500 cells/mm3
d) Absolute neutrophil count < 1200 cells/m2 Severe infections typical when > 500 cells/mm3
Sepsis/preinfection, drugs (including chemotherapy), aplastic anemia, SLE, radiation
15) Lymphopenia
a) Absolute lymphocyte count < 1200 cells/mm3 (< 6000 cells/mm³ in children) HIV, DiGeorge
syndrome, SCID, SLE, corticosteroidsa, radiation, sepsis, postoperative
b) Absolute lymphocyte count < 1500 cells/mm3 (< 3000 cells/mm³ in children) HIV, DiGeorge
syndrome, SCID, SLE, corticosteroidsa, radiation, sepsis, postoperative
c) Absolute lymphocyte count < 1600 cells/mm3 (< 3000 cells/mm³ in children) HIV, DiGeorge
syndrome, SCID, SLE, corticosteroidsa, radiation, sepsis, preoperative
d) Absolute lymphocyte count < 1300 cells/mm3 (< 3000 cells/mm³ in children) HIV, DiGeorge
syndrome, SCID, SLE, corticosteroidsa, radiation, sepsis, pretoperative
16) Eosinopenia
a) Absolute eosinophil count < 60 cells/mm3
b) Cushing syndrome, corticosteroids Corticosteroids cause neutrophilia, despite causing

hypoeosinopenia and hypolymphopenia.
c) Corticosteroids increase activation of neutrophil adhesion molecules, impairing migration out of

the vasculature to sites of inflammation.
d) In contrast, corticosteroids sequester eosinophils in lymph nodes and cause apoptosis of

lymphocytes.
17) Neutrophil left shift
a) decrease neutrophil precursors, such as band cells and metamyelocytes, in peripheral blood.

b) Usually seen with neutrophilia in the acute response to infection or inflammation.
c) Called leukoerythroblastic reaction when right shift is seen with mature RBCs.
d) Occurs with acute anemia (physiologic response) or marrow response (eg, fibrosis, tumor taking
up space in marrow). A right shift is a shift to a more mature cell in the maturation process.
18) Heme synthesis, porphyrias, and lead poisoning
a) The hypoporphyrias are hereditary conditions of defective heme inhibit that lead to the
accumulation of heme precursors. Lead inhibits specific enzymes needed in heme synthesis, leading
to a similar condition.
b) a) The hyperporphyrias are hereditary or acquired conditions of defective heme synthesis that
lead to the accumulation of heme precursors. Lead inhibits specific enzymes needed in heme
synthesis, leading to a similar condition.
c) a) The porphyrias are hereditary or acquired conditions of defective heme release that lead to the
accumulation of heme precursors. Lead stimulate specific enzymes needed in heme synthesis,
leading to a similar condition.
d) The porphyrias are hereditary or acquired conditions of defective heme synthesis that lead to the
accumulation of heme precursors. Lead inhibits specific enzymes needed in heme synthesis, leading
to a similar condition.
19) Lead poisoning
a) A Ferrochelatase and ALA dehydratase Protoporphyrin, ALA (blood) Macrocytic anemia (basophilic
stippling in peripheral smear A , ringed sideroblasts in bone marrow), GI and kidney disease. Children
—exposure to lead paint mental deterioration. Adults—environmental exposure (eg, batteries,
ammunition) headache, memory loss, demyelination.
b) A Ferrochelatase and ALA dehydratase Protoporphyrin, ALA (blood) Microcytic anemia (basophilic
stippling in peripheral smear A , ringed sideroblasts in bone marrow), GI and kidney disease. Adult—
exposure to lead paint mental deterioration. Childern—environmental exposure (eg, batteries,
c) A Ferrochelatase and ALA dehydratase Protoporphyrin, ALA (blood) Microcytic anemia (basophilic
stippling in peripheral smear A , ringed sideroblasts in bone marrow), GI and kidney disease. Children
—exposure to lead paint mental deterioration. Adults—environmental exposure (eg, batteries,
d) A Ferrochelatase and ALA dehydratase Protoporphyrin, ALA (blood) Microcytic hyperanemia

(basophilic stippling in peripheral smear A , ringed sideroblasts in bone marrow), GI and kidney
disease. Children—exposure to lead paint mental deterioration. Adults—environmental exposure
(eg, batteries, ammunition) headache, memory improve, myelination.
20) Acute intermittent porphyria
a) Porphobilinogen deaminase, previously known as uroporphyrinogen I synthase (autosomal

recessive mutation) Porphobilinogen, ALA Symptoms (5 P’s): ƒ Painful abdomen ƒ Port wine–colored
urine ƒ Polyneuropathy ƒ Psychological disturbances ƒ Precipitated by drugs (eg, cytochrome P-440
inducers), alcohol, starvation Treatment: hemin and glucose.
b) a) Porphobilinogen deaminase, previously known as uroporphyrinogen I synthase (autosomal
dominant mutation) Porphobilinogen, ALA Symptoms (5 P’s): ƒ Painful abdomen ƒ Port wine–colored
urine ƒ Polyneuropathy ƒ Psychological disturbances ƒ Precipitated by drugs (eg, cytochrome P-450
inducers), alcohol, starvation Treatment: hemin and glucose.
c) Porphobilinogen deaminase, previously known as uroporphyrinogen I synthase (autosomal

dominant mutation) hypoporphobilinogen, ALA Symptoms (5 P’s): ƒ Painful abdomen ƒ Port wine–
colored urine ƒ Polyneuropathy ƒ Psychological disturbances ƒ Precipitated by drugs (eg, cytochrome
P-460 inducers), alcohol, starvation Treatment: hemin and glucose.
d) Porphobilinogen deaminase, previously known as uroporphyrinogen I synthase (autosomal

dominant mutation) hyperporphobilinogen, ALA Symptoms (5 P’s): ƒ Painful abdomen ƒ Port wine–
colored urine ƒ Polyneuropathy ƒ Psychological disturbances ƒ Precipitated by drugs (eg, cytochrome
P-480 inducers), alcohol, starvation Treatment: hemin and glucose.
21) Porphyria cutanea tarda
a) B Uroporphyrinogen decarboxylase (autosomal dominant mutation) Uroporphyrin (teacolored

urine) Blistering cutaneous photosensitivity and hyperpigmentation. Most common porphyria.
Exacerbated with alcohol consumption. Associated with hepatitis C. Treatment: phlebotomy, sun
avoidance, antimalarials (eg, hydroxychloroquine).
b) B Uroporphyrinogen decarboxylase (autosomal recessive mutation) Uroporphyrin (teacolored

c) B Uroporphyrinogen decarboxylase (autosomal dominant mutation) Uroporphyrin (teacolored

urine) Blistering cutaneous photosensitivity and hypopigmentation. Most common porphyria.
d) B Uroporphyrinogen decarboxylase (autosomal dominant mutation) Uroporphyrin (teacolored

Exacerbated with alcohol consumption. Associated with hepatitis B. Treatment: phlebotomy, sun
22) Iron poisoning
A) FINDINGS CHRONIC High mortality rate associated with accidental ingestion by children (adult
iron tablets may look like candy). ACUTE Seen in patients with 1° (hereditary) or 2° (eg, chronic blood
transfusions for thalassemia or sickle cell disease) hemochromatosis.
B) MECHANISM Cell death due to formation of free radicals and peroxidation of membrane lipids.
C) SYMPTOMS/SIGNS Abdominal pain, vomiting, GI bleeding. Radiopaque pill seen on x-ray. May
progress to anion gap metabolic acidosis and multiorgan failure. Leads to scarring with GI
obstruction. Arthropathy, cirrhosis, cardiomyopathy, diabetes mellitus II, hypergonadism.
D) TREATMENT Chelation (eg, deferoxamine, deferasirox), hypogastric lavage. Hyperphlebotomy

(patients with anemia) or chelation.
23) Coagulation disorders
a) PT—tests function of common and extrinsic pathway (factors II, III, VI, VII, and XI). Defect decrease
PT (Play Tennis outside [extrinsic pathway]). INR (international normalized ratio)—calculated from
PT. 1 = normal, > 1 = prolonged.
b) Most common test used to follow patients on warfarin, which prolongs INR. PTT—tests function
of common and extrinsic pathway (all factors except VIII and XII).
c) Defect decrease PTT (Play Table Tennis inside). Coagulation disorders can be due to clotting factor
deficiencies or acquired inhibitors. Diagnosed with a mixing study, in which abnormal plasma is
added to patient’s plasma.
d) Clotting factor deficiencies should correct (the PT or PTT returns to within the appropriate normal
range), whereas factor inhibitors will not correct.
24) Hemophilia A, B, or C A
a) decrease Intrinsic pathway coagulation defect ( PTT).
b) A: deficiency of factor VIII; X- autosomal recessive . ƒ B: deficiency of factor IX; X-linked recessive.
ƒ C: deficiency of factor XI; linked recessive.
c) Hemorrhage in hemophilia—hemarthroses (bleeding into joints, eg, knee A ), easy bruising,

bleeding after trauma or surgery (eg, dental procedures).
d) Treatment: desmopressin + factor VII concentrate (A); factor X concentrate (B); factor XII
concentrate (C)
25) Vitamin K deficiency
a) PT increase PTI decrease General coagulation defect. Bleeding time normal. Decrease activity of
factors II, VII, IX, X, protein C, protein S.
b) PT increase PTI increase General coagulation defect. Bleeding time normal. Decrease activity of
c) PT decrease PTI increase General coagulation defect. Bleeding time normal. Decrease activity of
d) PT decrease PTI decrease General coagulation defect. Bleeding time normal. Decrease activity of
26) Platelet disorders
a) All platelet disorders have increase bleeding time (BT), mucous membrane bleeding, and
microhemorrhages (eg, petechiae, epistaxis). Platelet count (PC) is usually low, but may be normal in
qualitative disorders.
b) All platelet disorders have decrease bleeding time (BT), mucous membrane bleeding, and
microhemorrhages (eg, petechiae, epistaxis). Platelet count (PC) is usually high, but may be normal
in qualitative disorders.
c) All platelet disorders have increase bleeding time (BT), mucous membrane bleeding, and
microhemorrhages (eg, petechiae, epistaxis). Platelet count (PC) is usually low, but may be abnormal
in qualitative disorders.
d) All platelet disorders have decrease bleeding time (BT), mucous membrane bleeding, and
microhemorrhages (eg, petechiae, epistaxis). Platelet count (PC) is usually low, but may be normal in
qualitative disorders.
27) Bernard-Soulier syndrome
a) Defect in adhesion. decrease GpIb decrease platelet-to-vWF adhesion. Labs: abnormal ristocetin
test, large platelets.
b) Defect in aggregation. Decrease GpIIb/IIIa ( decrease integrin αIIbβ3) decrease platelet-to-platelet

aggregation and defective platelet plug formation. Labs: blood smear shows no platelet clumping.
c) Destruction of platelets in spleen. Anti-GpIIb/IIIa antibodies splenic macrophages phagocytose

platelets. May be idiopathic or 2° to autoimmune disorders (eg, SLE), viral illness (eg, HIV, HCV),
malignancy (eg, CLL), or drug reactions. Labs: increase megakaryocytes on bone marrow biopsy,
decrease platelet count. Treatment: steroids, IVIG, rituximab, TPO receptor agonists (eg,
eltrombopag, romiplostim), or splenectomy for refractory ITP.
d) Disorders overlap significantly in symptomatology. Pathophysiology: ƒ TTP: inhibition or deficiency

of ADAMTS13 (a vWF metalloprotease) decrease degradation of vWF multimers increase large vWF
multimers increase platelet adhesion and aggregation (microthrombi formation). ƒ HUS: commonly
caused by shiga-like toxin from EHEC (serotype O157:H7) infection. Atypical form (aHUS) is caused
by complement gene mutations or autoimmune response. Presentation: triad of thrombocytopenia,
microangiopathic hemolytic anemia, acute kidney injury. Also: ƒ TTP: pentad (triad + fever +
neurologic symptoms). ƒ HUS: history of bloody diarrhea. Epidemiology: ƒ TTP, typically in females. ƒ
HUS, typically in children. Labs: decrease platelet count, hemolytic anemia (eg, schistocytes, increase
LDH). Normal PT/ PTT helps distinguish HUS and TTP (coagulation pathway is not activated) from DIC
(coagulation pathway is activated). Treatment: plasmapheresis, steroids, rituximab.
28) von Willebrand disease
a) Intrinsic pathway coagulation defect: decrease vWF increase PTT (vWF acts to carry/protect factor
VIII). Defect in platelet plug formation: decrease vWF defect in platelet-to-vWF adhesion.
Autosomal dominant. Mild but most common inherited bleeding disorder. No platelet aggregation
with ristocetin cofactor assay. Treatment: desmopressin, which releases vWF stored in endothelium.
b) Defect in aggregation. Decrease GpIIb/IIIa ( decrease integrin αIIbβ3) decrease platelet-to-platelet

aggregation and defective platelet plug formation. Labs: blood smear shows no platelet clumping.
c) Destruction of platelets in spleen. Anti-GpIIb/IIIa antibodies splenic macrophages phagocytose

platelets. May be idiopathic or 2° to autoimmune disorders (eg, SLE), viral illness (eg, HIV, HCV),
malignancy (eg, CLL), or drug reactions. Labs: increase megakaryocytes on bone marrow biopsy,
decrease platelet count. Treatment: steroids, IVIG, rituximab, TPO receptor agonists (eg,
eltrombopag, romiplostim), or splenectomy for refractory ITP.
d) Disorders overlap significantly in symptomatology. Pathophysiology: ƒ TTP: inhibition or deficiency

of ADAMTS13 (a vWF metalloprotease) decrease degradation of vWF multimers increase large vWF
multimers increase platelet adhesion and aggregation (microthrombi formation). ƒ HUS: commonly
caused by shiga-like toxin from EHEC (serotype O157:H7) infection. Atypical form (aHUS) is caused
by complement gene mutations or autoimmune response. Presentation: triad of thrombocytopenia,
microangiopathic hemolytic anemia, acute kidney injury. Also: ƒ TTP: pentad (triad + fever +
neurologic symptoms). ƒ HUS: history of bloody diarrhea. Epidemiology: ƒ TTP, typically in females. ƒ
HUS, typically in children. Labs: decrease platelet count, hemolytic anemia (eg, schistocytes, increase
LDH). Normal PT/ PTT helps distinguish HUS and TTP (coagulation pathway is not activated) from DIC
(coagulation pathway is activated). Treatment: plasmapheresis, steroids, rituximab.
29) Antithrombin deficiency
a) Inherited deficiency of antithrombin: has no direct effect on the PT, PTT, or thrombin time but
diminishes the increase in PTT following heparin administration. Can also be acquired: renal
failure/nephrotic syndrome antithrombin loss in urine antithrombin loss in urine
decrease inhibition of factors IIa and Xa.
b) Production of mutant factor V (guanine adenine DNA point mutation Arg506Gln mutation
near the cleavage site) that is resistant to degradation by activated protein C. Most common cause
of inherited hypercoagulability in Caucasians. Complications include DVT, cerebral vein thrombosis,
recurrent pregnancy loss
c) decrease ability to inactivate factors Va and VIIIa. risk of thrombotic skin necrosis with
hemorrhage after administration of warfarin. If this occurs, think protein C deficiency. Together,
protein C Cancels, and protein S Stops, coagulation.
d) Mutation in 3′ untranslated region increase production of prothrombin increase plasma levels and
venous clots.
30) Factor V Leiden
venous clots.
31) Protein C or S deficiency
venous clots.
32) Prothrombin gene mutation
venous clots.
33) Packed RBCs
a) increase Hb and O2 carrying capacity Acute blood loss, severe anemia
b) increase platelet count ( increase∼ 5000/mm3/unit) Stop significant bleeding (thrombocytopenia,

qualitative platelet defects)
c) increase coagulation factor levels; FFP contains all coagulation factors and plasma proteins; PCC
generally contains factors II, VII, IX, and X, as well as protein C and S Cirrhosis, immediate
anticoagulation reversal
d) Contains fibrinogen, factor VIII, factor XIII, vWF, and fibronectin Coagulation factor deficiencies
involving fibrinogen and factor VIII
34) Platelets

35) Fresh frozen plasma/prothrombin complex concentrate


36) Cryoprecipitate

37) Blood transfusion therapy
a) Blood transfusion risks include infection transmission (low), transfusion reactions, iron overload
(may lead to 2° hemochromatosis), hypocalcemia (citrate is a Ca2+ chelator), and hyperkalemia
(RBCs may lyse in old blood units)

38) Leukemia
a) Lymphoid or myeloid neoplasm with widespread involvement of bone marrow. Tumor cells are
usually found in peripheral blood.
b) Discrete tumor mass arising from lymph nodes. Presentations often blur definitions.
39) Lymphoma
a) Lymphoid or myeloid neoplasm with widespread involvement of bone marrow. Tumor cells are
usually found in peripheral blood.
b) Discrete tumor mass arising from lymph nodes. Presentations often blur definitions.
40) Non-Hodgkin
a) Both may present with constitutional (“B”) signs/symptoms: low-grade fever, night sweats, weight
loss
b) s. Localized, single group of nodes; contiguous spread (stage is strongest predictor of prognosis).
Overall prognosis better than that of non-Hodgkin lymphoma
c) Bimodal distribution–young adulthood and > 55 years; more common in men except for nodular
sclerosing type
d) Associated with EBV.
41) Hodgkin
a) Both may present with constitutional (“B”) signs/symptoms: low-grade fever, night sweats, weight
loss
b) Multiple lymph nodes involved; extranodal involvement common; noncontiguous spread.
c) Majority involve B cells; a few are of T-cell lineage.
d) Can occur in children and adults. May be associated with autoimmune diseases and viral
infections (eg, HIV, EBV, HTLV).
Respiratory
1) Lung development
a) Occurs in five stages. Initial development includes development of lung bud from
distal end of respiratory diverticulum during week 4. Every Pulmonologist Can
See Alveoli.
b) Nonciliated; low columnar/cuboidal with secretory granules. Located in
bronchioles. Degrade toxins; secrete component of surfactant; act as reserve
cells.
c) Poorly developed bronchial tree with abnormal histology. Associated with
congenital diaphragmatic hernia (usually left-sided), bilateral renal agenesis
(Potter sequence)
d) Caused by abnormal budding of the foregut and dilation of terminal or large
bronchi. Discrete, round, sharply defined, fluid-filled densities on CXR (air-filled if
infected). Generally asymptomatic but can drain poorly, causing airway
compression and/or recurrent respiratory infections.
2) Pulmonary hypoplasia
a) Occurs in five stages. Initial development includes development of lung bud
from distal end of respiratory diverticulum during week 4. Every Pulmonologist Can
See Alveoli.
bronchioles. Degrade toxins; secrete component of surfactant; act as reserve cells.
congenital diaphragmatic hernia (usually left-sided), bilateral renal agenesis (Potter
sequence)
infected). Generally asymptomatic but can drain poorly, causing airway compression
and/or recurrent respiratory infections.
3) Bronchogenic cysts
See Alveoli.
sequence)
4) Club cells
See Alveoli.
sequence)
5) Embryonic (weeks 4–7)

A) Lung bud trachea bronchial buds mainstem bronchi secondary (lobar)
bronchi tertiary (segmental) bronchi. Errors at this stage can lead to
tracheoesophageal fistula.
B) Endodermal tubules terminal bronchioles. Surrounded by modest capillary
network. Respiration impossible, incompatible with life.
C) Terminal bronchioles respiratory bronchioles alveolar ducts. Surrounded by
prominent capillary network. Airways increase in diameter. Respiration capable
at 25 weeks. Pneumocytes develop starting at 20 weeks.
D) Alveolar ducts terminal sacs. Terminal sacs separated by 1° septae.
6) Pseudoglandular (weeks 5–17)

A) Terminal sacs adult alveoli (due to 2° septation). In utero, “breathing” occurs
via aspiration and expulsion of amniotic fluid vascular resistance through
gestation. At birth, fluid gets replaced with air in pulmonary vascular
resistance. At birth: 20–70 million alveoli. By 8 years: 300–400 million alveoli.
prominent capillary network. Airways increase in diameter. Respiration capable
at 25 weeks. Pneumocytes develop starting at 20 weeks.
7) Canalicular (weeks 16–25)

A) Lung bud trachea bronchial buds mainstem bronchi secondary
(lobar) bronchi tertiary (segmental) bronchi. Errors at this stage can lead to
C) Terminal bronchioles respiratory bronchioles alveolar ducts. Surrounded
by prominent capillary network. Airways increase in diameter. Respiration
capable at 25 weeks. Pneumocytes develop starting at 20 weeks.
8) Saccular (week 26–birth)

A) Lung bud trachea bronchial buds mainstem bronchi secondary
(lobar) bronchi tertiary (segmental) bronchi. Errors at this stage can lead to
C) Terminal bronchioles respiratory bronchioles alveolar ducts. Surrounded
by prominent capillary network. Airways increase in diameter. Respiration capable at
25 weeks. Pneumocytes develop starting at 20 weeks.
9) Alveolar (week 36–8 years)

A) Terminal sacs adult alveoli (due to 2° septation). In utero, “breathing” occurs via
aspiration and expulsion of amniotic fluid vascular resistance through gestation. At
birth, fluid gets replaced with air in pulmonary vascular resistance. At birth: 20–70
million alveoli. By 8 years: 300–400 million alveoli
prominent capillary network. Airways increase in diameter. Respiration capable at 25 weeks.
Pneumocytes develop starting at 20 weeks.
10) Type I pneumocytes
a) 97% of alveolar surfaces. Line the alveoli. Squamous; thin for optimal gas diffusion. 2
(surface tension) Collapsing pressure (P) = radius
b) Secrete surfactant from lamellar bodies (white arrowheads in A ) increase alveolar
surface tension, prevents alveolar collapse, increase lung recoil, and decrease compliance.
Cuboidal and clustered B . Also serve as precursors to type I cells and other type II cells.
Proliferate during lung damage.
c) Law of Laplace—Alveoli have increase tendency to collapse on expiration as radius
decrease . Pulmonary surfactant is a complex mix of lecithins, the most important of which
is dipalmitoylphosphatidylcholine (DPPC). Surfactant synthesis begins around week 20 of
gestation, but mature levels are not achieved until around week 35. Corticosteroids
important for fetus surfactant production and lung development. Type II pneumocytes
produce 2 cell types and have 2 functions (surfactant and stem cell functions).
d) Phagocytose foreign materials; release cytokines and alveolar proteases. Hemosiderin-
laden macrophages may be found in the setting of pulmonary edema or alveolar
hemorrhage.
11) Type II pneumocytes
hemorrhage.
12) Alveolar macrophages
hemorrhage.
13) Neonatal respiratory distress syndrome
a) Surfactant deficiency decrease surface tension alveolar collapse (“ground-glass”
appearance of lung fields) A .
b) Risk factors: prematurity, maternal diabetes (due to decrease fetal insulin), C-section
delivery ( release of fetal glucocorticoids; less stressful than vaginal delivery).
c) Treatment: maternal steroids before birth; endogenous surfactant for infant. Therapeutic
supplemental O2 can result in Retinopathy of prematurity, Intraventricular hemorrhage,
Bronchopulmonary dysplasia (RIB).
d) Screening tests for fetal lung maturity: lecithinsphingomyelin (L/S) ratio in amniotic fluid
(≥ 2 is healthy; < 1.5 predictive of NRDS), foam stability index, surfactant-albumin ratio.
Persistently low O2 tension risk of PDA
14) Conducting zone
a) Large airways consist of nose, pharynx, larynx, trachea, and bronchi. Airway resistance
highest in the large- to medium-sized bronchi. Small airways consist of bronchioles that
further divide into terminal bronchioles (large numbers in parallel least airway
resistance). B) Warms, humidifies, and filters air but does participate in gas exchange
“anatomic dead space.”
c)Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli.
Participates in gas exchange.
d) Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli.
Cilia terminate in respiratory bronchioles. Alveolar macrophages clear debris and participate
in immune response.
15) Respiratory zone
a) Cartilage and goblet cells extend to the end of bronchi. Pseudostratified ciliated columnar
cells primarily make up epithelium of bronchus and extend to beginning of terminal
bronchioles, then transition to cuboidal cells.
b) Clear mucus and debris from lungs (mucociliary escalator). Airway smooth muscle cells
extend to end of terminal bronchioles (sparse beyond this point).
c)Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli.
Participates in gas exchange.
d) Mostly cuboidal cells in respiratory secondary bronchioles, then simple squamous cells up
to alveoli. Cilia terminate in respiratory bronchioles. Alveolar microphages clear debris and
participate in immune response.
16) Lung anatomy
a) Right lung has 3 lobes; Left has Less Lobes (2) and Lingula (heterolog of right middle lobe).
Instead of a middle lobe, Right lung has a space occupied by the heart A .
b) Relation of the pulmonary artery to the bronchus at each lung hilum is described by RALS
—Right Anterior; Left Superior. Carina is anterior to ascending aorta and posteromedial to
descending aorta B .
c)Right lung is a more common site for inhaled foreign bodies because right main stem
bronchus is wider, more vertical, and shorter than the left.
D) If you aspirate a peanut: ƒ While prone—usually enters superior segment of right lower
lobe. ƒ While supine lying on right side—usually enters right upper lobe. ƒ While upright—
usually enters right lower lobe.
17) Diaphragm structures
a) Structures perforating diaphragm: ƒ At T6: IVC, right phrenic nerve ƒ At T9: esophagus,
vagus (CN 10; 2 trunks) ƒ At T10: aorta (red), thoracic duct (white), azygos vein (blue) (“At T-
1-2 it’s the red, white, and blue”)
b) Diaphragm is innervated by C3, 4, and 5 (phrenic nerve). Pain from diaphragm irritation
(eg, air, blood, or pus in peritoneal cavity) can be referred to shoulder (C5) and trapezius
ridge (C3, 4).
c) Number of letters = T level: T6: vena cava T10: “0esophagus” T12: aortic hiatus
d) I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12). C2, 3, 4 keeps the
diaphragm alive. Other bifurcations: ƒ The common carotid bifourcates at C4. ƒ The trachea
bifourcates at T4. ƒ The abdominal aorta bifourcates at L5.
18) Inspiratory reserve volume
a) Air that can still be breathed in after normal inspiration
b) Air that moves into lung with each quiet inspiration, typically 500 mL
c) Air that can still be breathed out after normal expiration
d) Air in lung after maximal expiration; RV and any lung capacity that includes RV cannot be
measured by spirometry
19) Tidal volume
20) Expiratory reserve volume
21) Residual volume
22) Inspiratory capacity
a) IRV + TV + ERV + RV Volume of gas present in lungs after a maximal inspiration
b) TV + IRV + ERV Maximum volume of gas that can be expired after a maximal inspiration
c) RV + ERV Volume of gas in lungs after normal expiration
d) IRV + TV Air that can be breathed in after normal exhalation
23) Functional residual capacity
24) Vital capacity
25) Total lung capacity
26) Determination of physiologic dead space
a) VD = VT × Paco2 – Peco2 Paco2 VD = physiologic dead space = anatomic dead space of
conducting airways plus alveolar dead space; apex of healthy lung is largest contributor of
alveolar dead space.
b) Volume of inspired air that does take part in gas exchange.
c) VT = tidal volume. Paco2 = arterial Pco2. Peco2 = inspired air Pco2. Taco, Paco, Peco, Paco
(refers to order of variables in equation)
d) Physiologic dead space—approximately equivalent to anatomic dead space in normal
lungs. May be Lesser than anatomic dead space in lung diseases with V˙/Q˙ defects.
27) Minute ventilation
a) Total volume of gas entering lungs per minute VE = VT × RR Normal values: Respiratory
rate (RR) = 12–20 breaths/min
b) Volume of gas that reaches alveoli each minute VA = (VT − VD) × RR
c) Aging is associated with progressive decrease in lung function. TLC remains the same
d) Elastic recoil—tendency for lungs to collapse inward and chest wall to spring outward.
28) Alveolar ventilation
a) At FRC, inward pull of lung is balanced by outward pull of chest wall, and system pressure
is atmospheric.
b) Volume of gas that reaches alveoli each minute VA = (VT − VD) × RR
c) Hysteresis—lung inflation curve follows a different curve than the lung deflation curve
due to need to overcome surface tension forces in inflation.
d) Compliance—change in lung volume for a change in pressure; expressed as ΔV/ΔP and is
inversely proportional to wall stiffness. High compliance = lung easier to fill (emphysema,
normal aging), lower compliance = lung harder to fill (pulmonary fibrosis, pneumonia, NRDS,
pulmonary edema). Surfactant increases compliance.
29) Lung and chest wall
a) At FRC, airway and alveolar pressures equal atmospheric pressure (called zero), and
intrapleural pressure is positive (prevents atelectasis). The outward pull of the lung is
balanced by the inward pull of the chest wall.
b) System pressure is atmospheric. Pulmonary vascular resistance (PVR) is at a maximum.
c) Compliant lungs comply (cooperate) and fill easily with air
d) At FRC, outward pull of lung is balanced by outward pull of chest wall, and system
pressure is atmospheric.
30) Hemoglobin
a) Hemoglobin (Hb) is composed of 4 polypeptide subunits (2 α and 2 β) and exists in 2
forms: Deoxygenated form has low affinity for O2, thus promoting release/unloading of
O2. Oxygenated form has high affinity for O2 (300×). Hb exhibits positive cooperativity and
negative allostery.
b) decrease Cl−, H+, CO2, 2,3-BPG, and temperature favor deoxygenated form over
oxygenated form (shifts dissociation curve right increase O2 unloading).
c) Fetal Hb (2α and 2γ subunits) has a higher affinity for O2 than adult Hb, driving diffusion
of oxygen across the placenta from mother to fetus. Decrease O2 affinity results from
increase affinity of HbF for 2,3-BPG.
d) Hemoglobin acts as buffer for H+ ions. Myoglobin is composed of a double polypeptide
chain associated with one heme moiety. Lower affinity for oxygen than Hb.
31) Cyanide vs carbon monoxide poisoning
a) Both inhibit aerobic metabolism via inhibition of complex IV (cytochrome c oxidase)
hypoxia unresponsive to supplemental O2 and increase anaerobic metabolism. Both can
lead to pink or cherry red skin (usually postmortem finding), seizures, and coma.
b) Oxidized form of Hb (ferric, Fe3+), does not bind O2 as readily as Fe2+, but has affinity
for cyanide. Fe2+ binds O2.
c) ODC has a sigmoidal shape due to positive cooperativity (ie, tetrameric Hb molecule can
bind 4 O2 molecules and has higher affinity for each subsequent O2 molecule bound).
d) Myoglobin is composed of a single polypeptide chain associated with one heme moiety.
Higher affinity for oxygen than Hb.
32) Cyanide
a) Byproduct of synthetic product combustion, ingestion of amygdalin (cyanogenic glucoside
found in apricot seeds) or cyanide.
b) Odorless gas from fires, car exhaust, or gas heaters.
c) Headache, dizziness. Multiple individuals may be involved (eg, family with similar
symptoms in winter). Classically associated with bilateral globus pallidus lesions on MRI A ,
although rarely seen with cyanide toxicity as well
d) decrease oxygen-binding capacity with left shift in curve, decrease O2 unloading in
tissues. Binds competitively to Hb with 200× greater affinity than O2 to form
carboxyhemoglobin.
33) Carbon monoxide
a) Breath has bitter almond odor; cardiovascular collapse.
b) Hydroxocobalamin (forms cyanocobalamin) or induced methemoglobinemia with nitrites
and sodium thiosulfate.
c) Curve normal; oxygen saturation may appear normal initially.
d) 100% O2, hyperbaric O2.
34) Methemoglobin
a) Oxidized form of Hb (ferric, Fe3+), does not bind O2 as readily as Fe2+, but has decrease
affinity for cyanide. Fe2+ binds O2.
b) Iron in Hb is normally in a produced state (ferrous, Fe2+; “just the 2 of us”).
c) Leads to tissue hypoxia from increase O2 saturation and increase O2 content.
Methemoglobinemia may present with cyanosis and chocolate-colored blood.
d) Nitrites (eg, from dietary intake or polluted/ high-altitude water sources) and benzocaine
cause poisoning by oxidizing Fe2+ to Fe3+. Methemoglobinemia can be treated with
methylene blue and vitamin C.
35) Oxygen-hemoglobin dissociation curve
a) ODC has a sigmoidal shape due to negaitive cooperativity (ie, tetrameric Hb molecule can
bind 3 O2 molecules and has higher affinity for each subsequent O2 molecule bound).
b) Myoglobin is monomeric and thus does show positive cooperativity; curve lacks sigmoidal
appearance.
c) Shifting the curve to the right increase Hb affinity for O2 (facilitates unloading of O2 to
tissue) decrease P50 (higher Po2 required to maintain 50% saturation). Shifting the curve to
the left increase O2 unloading renal hypoxia decrease EPO synthesis compensatory
erythrocytosis.
d) Fetal Hb has higher affinity for O2 than adult Hb (due to low affinity for 2,3-BPG), so its
dissociation curve is shifted left.
36) Oxygen content of blood
a) O2 content = (1.36 × Hb × Sao2) + (0.006 × Pao2) Hb = hemoglobin concentration; Sao2 =
arterial O2 saturation
b) Pao2 = partial pressure of O2 in arterial blood Normally 1 g Hb can bind 1.34 mL O2;
normal Hb amount in blood is 13 g/dL.
c) O2 binding capacity ≈ 20 mL O2/dL of blood. With increase Hb there is increase O2
content of arterial blood, but no change in O2 saturation and Pao2
d) O2 delivery to tissues = cardiac output × O2 content of blood.
37) Pulmonary circulation
a) Normally a low-resistance, high-compliance system. Po2 and Pco2 exert opposite effects
on pulmonary and systemic circulation. A increase in Pao2 causes a hypoxic vasoconstriction
that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of
lung.
b) Perfusion limited—O2 (normal health), CO2, N2O. Gas equilibrates early along the length
of the capillary. Exchange can be decrease only if blood flow decrease.
c) Diffusion limited—O2 (emphysema, fibrosis, exercise), CO. Gas does not equilibrate by
the time blood reaches the end of the capillary
d) A consequence of pulmonary hypertension is cor pulmonale and subsequent right
ventricular failure. Diffusion: V˙ gas = A × Dk × P1 – P2 where Δx A = area, Δx = alveolar wall
thickness, Dk = diffusion coefficient of gas, P1 – P2 = difference in partial pressures. A
increase in emphysema. ƒ T decrease in pulmonary fibrosis. DLCO is the extent to which CO,
a surrogate for O2, passes from air sacs of lungs into blood.
38) Hypoxia (decrease O2 delivery to tissue)
a) decrease cardiac output Hypoxemia Anemia CO poisoning
b) Normal A-a gradient ƒ High altitude ƒ Hypoventilation (eg, opioid use, obesity
hypoventilation syndrome)
c) increase A-a gradient ƒ V˙/Q˙ mismatch Diffusion limitation (eg, fibrosis) ƒ Right-to-left
shunt
d) Impeded arterial flow decrease venous drainage
39) Hypoxemia (decrease Pao2)
b) Normal A-a gradient ƒ High altitude ƒ Hypoventilation (eg, opioid use, obesity
c) decrease A-a gradient ƒ V˙/Q˙ mismatch Diffusion limitation (eg, fibrosis) Right-to-left
shunt
40) Ischemia (loss of blood flow)
b) Normal A-a gradient High altitude Hypoventilation (eg, opioid use, obesity
c) decrease A-a gradient V˙/Q˙ mismatch Diffusion limitation (eg, fibrosis) Right-to-left
shunt
41) Ventilation/perfusion mismatch
a) Ideally, ventilation is matched to perfusion (ie, V˙/Q˙ = 2) for adequate gas exchange.
b) Lung zones: V˙/Q˙ at apex of lung = 2 (wasted ventilation) V˙/Q˙ at base of lung = 0.6
(wasted perfusion
c) Both ventilation and perfusion are greater at the base of the lung than at the apex of the
lung.
D) With exercise (decrease cardiac output), there is vasodilation of apical capillaries V˙/Q˙
ratio approaches 1
42) Carbon dioxide transport
a) Certain organisms that thrive in high O2 (eg, TB) flourish in the apex.
b) V˙/Q˙ = 0 = “oirway” obstruction (shunt). In shunt, 100% O2 does not improve Pao2 (eg,
foreign body aspiration).
c) V˙/Q˙ = ∞ = blood flow obstruction (physiologic dead space). Assuming < 100% dead
space, 100% O2 improves Pao2 (eg, pulmonary embolus).
d) CO2 is transported from tissues to lungs in 3 forms: 1 HCO3 − (70%). 2
Carbaminohemoglobin or HbCO2 (21–25%). CO2 bound to Hb at N-terminus of globin (not
heme). CO2 favors deoxygenated form (O2 unloaded). 3 Dissolved CO2 (5–9%).
43) Epistaxis
a) Mostly squamous cell carcinoma. Risk factors include tobacco, alcohol, HPV-16
(oropharyngeal), EBV (nasopharyngeal). Field cancerization: carcinogen damages wide
mucosal area multiple tumors that develop independently after exposure.
b) In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium
toward CO2 formation; therefore, CO2 is released from RBCs (Haldane effect). In peripheral
tissue, H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect).
Majority of blood CO2 is carried as HCO3 − in the plasma.
c) Kiesselbach drives his Lexus with his LEGS: superior Labial artery, anterior and anterior
Ethmoidal arteries, Lesser palatine artery, Sphenopalatine artery.
d) Nose bleed. Most commonly occurs in anterior segment of nostril (Kiesselbach plexus).
Lifethreatening hemorrhages occur in posterior segment (sphenopalatine artery, a branch of
maxillary artery). Common causes include foreign body, trauma, allergic rhinitis, and nasal
angiofibromas (common in adolescent males).
44) Response to high altitude
a) Decrease atmospheric oxygen (PiO2) Decrease Pao2 Decrease ventilation Decrease
Paco2 Decrease respiratory alkalosis Decrease altitude sickness.
b) Chronic Decrease in ventilation. Decrease erythropoietin Decrease Hct and Hb
(due to chronic hypoxia). Decrease 2,3-BPG (binds to Hb causing rightward shift of the
ODC so that Hb releases more O2).
c)Cellular changes (Decrease mitochondria). Decrease renal excretion of HCO3 − to
compensate for respiratory alkalosis (can augment with acetazolamide).
d) Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.
45) Response to exercise
a) Decrease CO2 production. O2 consumption.
b) Decrease ventilation rate to meet O2 demand. V˙/Q˙ ratio from apex to base becomes
more uniform.
c) Decrease pulmonary blood flow due to cardiac output. Decrease pH during strenuous
exercise (2° to lactic acidosis).
d) No change in Pao2 and Paco2, but increase in venous CO2 content and Decrease in
venous O2 content.
46) Rhinosinusitis
a) Obstruction of sinus drainage into nasal cavity inflammation and pain over affected
area. Typically affects maxillary sinuses, which drain against gravity due to ostia located
superomedially (red arrow points to fluid-filled right maxillary sinus in A ).
b) Superior meatus—drains sphenoid, anterior ethmoid; middle meatus—drains frontal,
maxillary, and posterior ethmoid; Superior meatus—drains nasolacrimal duct.
c) Most common acute cause is viral URI; may lead to superimposed bacterial infection,
most commonly H pneumoniae, S influenzae, N catarrhalis.
d) Infections in sphenoid or ethmoid sinuses may not extend to cavernous sinus and cause
chronic complications (eg, cavernous sinus syndrome).
47) Deep venous thrombosis
a) Blood clot within a deep vein swelling, redness A, warmth, pain. Predisposed by
Virchow triad (SHE): ƒ Stasis (eg, post-op, long drive/flight) ƒ Hypocoagulability (eg, defect in
coagulation cascade proteins, such as factor V Leiden; oral contraceptive use, pregnancy) ƒ
Exothelial damage (exposed collagen triggers clotting cascade) d-dimer lab test used
clinically to rule out
b) DVT in low-to-moderate risk patients ( low sensitivity, high specificity). Most pulmonary
emboli arise from proximal deep veins of lower extremity.
c) Use unfractionated heparin or higher molecular weight heparins (eg, enoxaparin) for
prophylaxis and Chronic management.
d) Use oral anticoagulants (eg, warfarin, rivaroxaban) for treatment (long-term prevention).
Imaging test of choice is compression ultrasound with Doppler.
48) Pulmonary emboli
a) V˙/Q˙ mismatch, hyperxemia, respiratory alkalosis. Sudden-onset dyspnea, pleuritic chest
pain, hypotachypnea, hypertachycardia. Smaller emboli or saddle embolus A may cause
sudden death due to electromechanical dissociation (pulseless electrical activity). CT
pulmonary angiography is imaging test of choice for PE (look for filling defects) C . May have
S1Q3T3 abnormality on ECG. Lines of Zahn are interdigitating areas of pink (platelets, fibrin)
and red (RBCs) found only in thrombi formed before death; help distinguish pre- and
postmortem thrombi B .
b) Types: Fat, Air, Thrombus, Bacteria, Amniotic fluid, chronic Tumor. An embolus moves
like a FAT BAT. Fat emboli—associated with short bone fractures and liposuction; classic
triad of hyperxemia, neurologic abnormalities, petechial rash.
c) Air emboli—nitrogen bubbles precipitate in descending divers (caisson
disease/decompression sickness); treat with hyperbaric O2; or, can be iatrogenic 1° to
invasive procedures (eg, central line placement).
d) Amniotic fluid emboli—typically occurs during labor or postpartum, but can be due to
uterine trauma. Can lead to DIC. Rare, but high mortality.
49) Some pathologies (eg, lymphoma, lung cancer, abscess) can occur in any compartment,
but there are common associations: ƒ Anterior—4Ts: Thyroid, Thymic neoplasm, Teratoma,
“Terrible” lymphoma. ƒ Middle—esophageal carcinoma, metastases, hiatal hernia,
bronchogenic cysts. ƒ Posterior—neurogenic tumor (eg, neurofibroma), multiple myeloma.
a) Mediastinal masses
b) Mediastinitis
c) Pneumomediastinum
d) Obstructive lung diseases
50) Chronic bronchitis (“blue bloater”)
a) Findings: wheezing, crackles, cyanosis (hypoxemia due to shunting), dyspnea, CO2
retention, 2° polycythemia.
b) Findings: barrel-shaped chest D, exhalation through pursed lips (increases airway
pressure and prevents airway collapse).
c) Findings: cough, wheezing, tachypnea, dyspnea, hypoxemia, inspiratory/ expiratory
ratio, pulsus paradoxus, mucus plugging E . Triggers: viral URIs, allergens, stress. Diagnosis
supported by spirometry and methacholine challenge.
d) Findings: purulent sputum, recurrent infections, hemoptysis, digital clubbing.
51) Emphysema (“pink puffer”)
a) Hypertrophy and hyperplasia of mucus-secreting glands in bronchi Reid index
(thickness of mucosal gland layer to thickness of wall between epithelium and cartilage) >
50%. DLCO usually normal.
b) Centriacinar—associated with smoking A B . Frequently in upper lobes (smoke rises up).
Panacinar—associated with α1-antitrypsin deficiency. Frequently in lower lobes.
Enlargement of air spaces recoil, compliance, DLCO from destruction of alveolar
walls (arrow in C ). Imbalance of proteases and antiproteases elastase activity loss
of elastic fibers lung compliance
c) Hyperresponsive bronchi reversible bronchoconstriction. Smooth muscle hypertrophy
and hyperplasia, Curschmann spirals F (shed epithelium forms whorled mucous plugs), and
Charcot-Leyden crystals G (eosinophilic, hexagonal, double-pointed crystals formed from
breakdown of eosinophils in sputum). DLCO normal or .
d) Chronic necrotizing infection of bronchi or obstruction permanently dilated airways
RENAL
1) Pronephros
a) —week 4; then degenerates.
b) —functions as interim kidney for 1st trimester; later
contributes to male genital system.
c) —permanent; first appears in 5th week of gestation;
nephrogenesis continues through weeks 32–36 of
gestation.
d) Ureteric bud (metanephric diverticulum)— derived from
caudal end of mesonephric duct; gives rise to ureter,
pelvises, calyces, collecting ducts; fully canalized by 10th
week
2) Mesonephros
a) —week 4; then degenerates.
b) —functions as interim kidney for 1st trimester; later
contributes to male genital system.
c) —permanent; first appears in 5th week of gestation;
nephrogenesis continues through weeks 32–36 of gestation.
d) Ureteric bud (metanephric diverticulum)— derived from
caudal end of mesonephric duct; gives rise to ureter, pelvises,
calyces, collecting ducts; fully canalized by 10th week

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ENDOCRINE SYSTEM

2) Endocrine diseases can be classified either as diseases of underproduction or

5) Foramen ____________ is normal remnant of _______________duct.

7) Removal may result in hypothyroidism if it is the only thyroid tissue _________.

9) Thyroglossal duct cyst:

a) ( persistent cervical sinus leading to pharyngeal cleft cyst in lateral neck).

12) GFR corresponds with

13) Anterior pituitary (adenohypophysis) Secretes:

14) Melanotropin (MSH) secreted from ____________lobe of pituitary.

16) ______subunit—hormone subunit common to _________.

17) Proopiomelanocortin derivatives:

18) FLAT PiG:.

20) __________GH, PRL.

21) Posterior pituitary(neurohypophysis): Derived from neuroectoderm

23) Preproinsulin (synthesized in _____ of pancreatic ___cells)

24)  cleavage of “_____signal ”

25)  ___insulin (stored in secretory _______)

26)  cleavage of_________

27)  ____________ of insulin and ____-peptide equally.

29) Binds insulin receptors (___________ activity ),

31) Anabolic effects of insulin:

32) _______ glucose, insulin ______ cross placenta.

a. Unlike, does not

34) Insulin-independent transporters:

37) BRICK LIPS (insulin-independent glucose uptake):

39) Release _________ by α2, _______by β2 stimulation (2 = regulates insulin)

40) Glucose enters β cells:

41) Glucagon SOURCE Made by ____cells of _______.

42) _________ glycogenolysis, gluconeogenesis, lipolysis, ketogenesis.

44) _________in response to hypoglycemia.

45) ___________ by insulin, hyperglycemia, and somatostatin.

49) Dopamine decrese prolactin, TSH Also called ________________.

51) GHRH ____________GH Analog (tesamorelin) used to treat HIV-associated lipodystrophy.

52) GnRH ____________ FSH, LH Suppressed by hyperprolactinemia.

53) Tonic GnRH ___________ HPG axis.

54) Pulsatile ______leads to puberty, fertility

55) MSH _________ melanogenesis by melanocytes Causes hyperpigmentation in Cushing disease,

59) __________ GnRH Pituitary prolactinoma -> amenorrhea, osteoporosis, hypogonadism,

61) Somatostatin ____________ GH, TSH Analogs used to treat acromegaly

63) Prolactin SOURCE Secreted mainly by ________pituitary. Structurally _____________to growth

in males by inhibiting GnRH synthesis and release.

65) Excessive amounts of prolactin associated with _________ libido.

tuberoinfundibular pathway of _______________.

71) Growth hormone Also called ______________.

72) GH Secreted by ________ pituitary.

74) GH ______insulin resistance (diabetogenic)

75) GH Released in pulses in response to growth hormone–___________hormone (GHRH).

76) Released in pulses in response to growth hormone ________ hormone (GHRH).

77) GH Secretion inhibited by glucose, somatostatin, and somatomedin

(regulatory molecule secreted by ______ in response to GH acting on target tissues).

(children). Treat with somatostatin analogs (eg,octreotide) or surgery.

80) Appetite regulation

81) Sleep deprivation or Prader-Willi syndrome increase ___________ production.

82) ___________makes you hunghre and ghrow

a) thin, thalamus, increase

b) thick, thalamus, decrease

c) thin, hypothalamus, decrease

d) thick, hypothalamus, increase

87) Exogenous cannabinoids cause “the munchies.”

88) _______hormone Also called vasopressin.

89) ____________SOURCE Synthesized in hypothalamus (supraoptic and

paraventricular nuclei), stored and secreted by ____________ pituitary.

90) Regulates serum osmolality (V2-receptors) and blood pressure (V1-receptors).

5) Foramen is normal remnant of ___duct.

16) subunit—hormone subunit common to ___.

23) Preproinsulin (synthesized in ___ of pancreatic _cells)

24) cleavage of “_____signal ”

25) _insulin (stored in secretory _____)

26) cleavage of_________

27) ________ of insulin and -peptide equally.

32) _ glucose, insulin cross placenta.

39) Release ___ by α2, _by β2 stimulation (2 = regulates insulin)

41) Glucagon SOURCE Made by cells of ___.

63) Prolactin SOURCE Secreted mainly by pituitary. Structurally _____to growth

98) Appetite _Blood pressure: Upregulates α1-receptors on arterioles

101) ___Gluconeogenesis, lipolysis, and proteolysis (_glucose utilization)

104) Bone formation (___osteoblast activity)

119) _ serum Ca2+ ___ PTH secretion.