Block 7 Exam Flashcards

1
Q

Negative Feedback

A

Goes back to earlier steps in the cascade to turn off hormone release

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2
Q

Positive feedback

A

Promoting a step later in the cascade pathway

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3
Q

Ligand

A

Any molecule that binds to a hormone receptor

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4
Q

Agonist

A

A hormone or synthetic ligand that activates hormone receptor function and signal transduction

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5
Q

Antagonist

A

A naturally occurring or synthetic ligand that prevents hormone receptor activation and signal transduction

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6
Q

EC50

A

Concentration of a hormone that attains half-maximal response

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7
Q

IC50

A

Concentration of an inhibitor at which the biological response is reduced by half

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8
Q

Kd

A

Concentration at which 50% of the binding sites are occupied by a hormone
Dissociation constant

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9
Q

High Kd

A

Low affinity

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10
Q

Low Kd

A

High affinity

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11
Q

Potency

A

Sensitivity

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12
Q

Efficacy

A

Responsiveness

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13
Q

Amino Acid-derived hormones

A
Dopamine (DA)
Epinephrine
Norepinephrine
Serotonin (5-HT)
Thyroid hormone (T3/T4)
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14
Q

Steroid hormone

A
Aldosterone
Cortisol
Estradiol (E2)
Progesterone
Testosterone
Vitamin D
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15
Q

Steroid hormone storage pools

A

none

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16
Q

Steroid hormone interaction w/ cell membrane

A

Diffusion through the membrane

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17
Q

Steroid hormone receptor location

A

cytoplasm or nucleus

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18
Q

Steroid hormone action

A

Regulation of gene transcription

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19
Q

Steroid hormone response time

A

Hours to days

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20
Q

Peptide and amine hormones storage pools

A

Secretory vesicles

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21
Q

Peptide and amine hormones interaction w/ cell membrane

A

binding to receptor on cell membrane

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22
Q

Peptide and amine hormones receptor location

A

Cell membrane

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23
Q

Peptide and amine hormones Action

A

Signal transduction cascades affecting a variety of cell processes

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24
Q

Peptide and amine hormones Response time

A

Seconds to minutes

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25
PTH Receptor
G-alpha s
26
ANGII receptor
G-alpha i | Gi/Go
27
AVP, ANGII, TRH receptor
G-alpha i
28
ANP receptor
Guanylyl cyclase
29
Insulin, IGF-1, IGF-2, EGF, PDGF receptor
Tyrosine kinase
30
GH, erythropoietin, LF
Tyrosine kinase associated receptor (Jak/Stat)
31
Possible responses
``` Transcription independent (immediate) Transcription dependent (delayed) ```
32
Hormones that use GPCR
Hypothalamus-derived "releasing" peptides Anterior pituitary-derived hormones Posterior pituitary-derived vasopressin and oxytocin Glucagon PTH, Calcitonin, and Ca2+ Epinephrine from adrenal medulla
33
Second messenger molecules
Cyclic nucleotides Lipids and lipid-derived breakdown products Ca2+ ions
34
Glucocorticoid receptor
GR/GR
35
Mineralocorticoid receptor
MR/MR
36
Thyroid hormone receptor
TR/RXR
37
Retinoic acid receptor
RAR/RXR
38
Hormones that use binding proteins
``` Thyroid hormone Glucocorticoids Estrogens Androgens Vitamin D Growth Hormones IGF1 and IGF2 ```
39
No binding proteins
``` Catecholamines PTH Calcitonin Glucagon Insulin ADH Renin ```
40
GHRH Target cell in anterior pituitary
Somatotroph
41
TRH Target cell in anterior pituitary
Thyrotroph
42
CRH Target cell in anterior pituitary
Corticotroph
43
GnRH Target cell in anterior pituitary
Gonadotroph and lactotroph
44
GHRH hormone released by anterior pituitary
GH
45
TRH hormone released by anterior pituitary
TSH
46
CRH hormone released by anterior pituitary
ACTH
47
GnRH hormone released by anterior pituitary
FSH LH PRL
48
Target of GH
Stimulates IGF-1 production
49
Target of TSH
Thyroid follicular cells, stimulated to make T3/T4
50
Target of ACTH
Fasiculata and reticularis cells of adrenal cortex, make corticosteroids
51
Target of FSH
Ovarian follicular cells, make estrogens and progestins | Sertoli cells, initiate spermatogenesis
52
Target of LH
Leydig cells, make testosterone
53
Target of PRL
Mammary glands, initiate and maintain milk production
54
AVP target
Collecting duct, increases water permeability
55
OT target
Uterus and breast
56
Autocrine
Cell stimulates self
57
Paracrine
Stimulates cell in close proximity
58
Juxtacrine
Stimulated cells immediately adjacent to the hormone-secreting cell
59
Endocine
Secretes hormone into the blood stream
60
Hierarchical control
Multiple control points | Brain involved
61
Simple feedback loop
No intervention from the brain
62
What are anterior pituitary hormones responsible for?
Reproduction Growth Energy metabolism Stress
63
What are the posterior pituitary hormones responsible for?
Water balance | Uterine contraction
64
Zona glomerulosa
Aldosterone synthesis
65
Zona Fasciculata
Glucocorticoid production
66
Zona Reticularis
Androgen production
67
Glucocorticoid function
Metabolism of carbohydrates and proteins
68
Mineralocorticoid function
Water balance and ECF volume
69
What is the rate limiting enzyme of adrenal steroid biosynthesis
SCC | Side chain cleaving enzyme
70
Cortisol hormone type
Steroid
71
Cortisol hormone class
glucocorticoid
72
Cortisol precursor
Cholesterol
73
Where is cortisol secreted
Fasciculata | Reticularis (minor)
74
Physiological effects of cortisol
``` Gluconeogenesis Proteolysis Lipolysis Immunosuppression Anti-inflammatory activity CNS differentiation/mood Differentiation of tissues Diuretic ```
75
Cortisol inhibitors
RU-486
76
Aldosterone hormone type
Steroid
77
Aldosterone hormone class
Mineralocorticoid
78
Aldosterone precursor
Cholesterol
79
Where is Aldosterone secreted
Glomerulusa
80
Aldosterone physiological effects
NaCl reabsorption via ENaCs | K+ excretion
81
Aldosterone inhibitors
Spironolactone
82
DHEA/Androgens hormone type
Steroid
83
DHEA/Androgens Hormone class
Sex/Androgen
84
DHEA/Androgens precursor
Cholesterol
85
Where are DHEA/Androgens secreted
Reticularis
86
DHEA/Androgens physiological effects
Masculinization Protein anabolism Growth
87
11 Beta-HSD1 location
Liver Adipocytes Placenta
88
11 Beta-HSD1 forward reaction
Cortisone => Cortisol
89
11 Beta-HSD1 reverse reaction
Cortisol => Cortisone
90
11 Beta-HSD2 location
Kidney
91
11 Beta-HSD2 reaction
Cortisol => Cortisone ONLY!
92
When is cortisol secretion highest?
8 AM
93
CRH GPCR
G-alpha s => Ca2+ influx
94
ACTH GPCR
G-alpha s => Increased activity of P-450 and synthesis of several enzymes
95
Major stimulation of aldosterone regulation
High serum K+ | ANGII
96
Minor stimulation of aldosterone regulation
ACTH
97
Cushing's Disease
Pituitary adenoma | Too much ACTH production => Excess cortisol production => Decreased CRH production
98
Cushing's syndrome
Excess cortisol
99
Addison's disease
Primary adrenal insufficiency | Too little cortisol => Increased levels of ACTH and cortisol
100
Adrenal adenoma or carcinoma (Cushing's syndrome)
Too much cortisol => Decreased CRH and ACTH
101
Ectopic CRH (Cushing's syndrome)
Tumor producing CRH => High ACTH => High cortisol | Low endogenous CRH
102
Primary disease
Last gland in HPA axis
103
Secondary disease
Pituitary gland
104
Tertiary disease
Hypothalamus
105
Cortisol effect on blood sugar
Raises | Promotes expression of gluconeogenic enzymes
106
Primary Hyper aldosteronism
Conn's syndrome Adrenal carcinoma/hyperplasia Lead to hypertension
107
Secondary hyperaldosteronism
Hypersecretion of aldosterone due to issue somewhere higher up in axis
108
What does hypersecretion of cortisol lead to
Hyperglycemia Decreased inflammatory response Muscle wasting Increased abdominal adipose tissue
109
Pseudo-Cushing's syndromes
Idiopathic | Obesity, depression, PCOS, diabetes, ALD
110
Hypersecretion of androgens can lead to:
Secondary male characteristics
111
Addison's disease | Primary hypoaldosteronism
Insufficient adrenal cortex function
112
What can Addison's disease lead to
``` Hypotension Weight loss Muscle weakness Fatigue Hyperpigmentation (increased POMC/ACTH) ```
113
Secondary hypoaldosteronism
Hyporeninemic hypoaldosteronism | Pseudo hypoaldosteronism
114
Why is norepinephrine not essential for life?
Released elsewhere
115
What enzyme is needed to convert Epi to NE
PNMT
116
A1-AR sensitivity efficacy
Epinephrine = Norepinephrine = ISO
117
A1-AR sensitivity potency
Epinephrine = Norepinephrine > ISO
118
Beta1-AR sensitivity efficacy
ISO = Epinephrine = Norepinephrine
119
Beta1-AR sensitivity potency
ISO > Epinephrine = Norepinephrine
120
Beta2-AR sensitivity efficacy
ISO = Epinephrine = Norepinephrine
121
Beta2-AR sensitivity potency
ISO > Epinephrine > Norepinephrine
122
Catecholamine function
Increased myocardial excitability Increased force and rate of contraction in the heart (beta-1) Vasoconstriction (alpha-1)
123
What intermediate is epinephrine converted to
Metanephrine
124
What intermediate is norepinephrine converted to
Normetanephrine
125
What are metanephrine and normetanephrine converted to
VMA by MAO
126
Pheochromocytoma
Life-threatening | Tumor of the adrenal medulla
127
Symptoms associated with sympathetic hypersensitivity
``` Tachycardia Headache Hypertension Hyperglycemia Gland enlargement ```
128
Environmental factors for obesity
``` Diet type (low fat vs high fat) Basal metabolism (UCP and neuropeptides) Level of hormones, cytokines, adipokines Quantity of sleep Microbiota Infectobesity ```
129
What do decreased leptin and adiponectin lead to
Increased food intake | Insulin resistance
130
UCP-1
Disrupts proton gradient
131
Regulation of Lipid Breakdown
Lipolysis is regulated by hormone sensitive lipase | Increase in cAMP activates lipase
132
Where is leptin produced
Adipocytes
133
Where is adiponectin produced
Adipocytes
134
Where is Ghrelin produced
Stomach
135
Where is CCK produced
Duodenum
136
What does leptin act on
Hypothalamus | Skeletal muscle
137
What does adiponectin act on
Systemic
138
What does Ghrelin act on
Hypothalamus
139
What does CCK act on
Stomach
140
Effect of leptin
Decrease food intake = feel full
141
Effect of adiponectin
Lowers blood glucose levels
142
Effect of Ghrelin
Promotes food intake
143
Effect of CCK
Decreases food intake
144
Effect of PYY
Decrease food intake | Results in weight loss
145
Effect of NPT neurons
Promotes food intake | Decrease in energy expenditure
146
Effect of POMC
Decreases food intake | Increases energy expenditure
147
What does PYY act on
Hypothalamus
148
What does NPY neurons act on
Hypothalamus
149
What does POMC act on
Hypothalamus | Brainstem
150
Where is PYY produced
Intestines
151
Where is NPY neurons produced
Hypothalamus
152
Where is POMC produced
Hypothalamus
153
Leptin and resistin
Induced by Feeding | Reduced by Fasting
154
Adiponectin
Positively correlated with insulin sensitivity
155
Plasma glucose fasting
60-80mg/dL | 3.3-4.4 mM
156
Plasma glucose Fed
100-140 mg/dL | 5.6-7.8 mM
157
What happens in the liver in a fasted state
Increase glycogenolysis Increase Gluconeogenesis Decrease Glycogen synthesis
158
What happens in the liver in a fed state
Decrease glycogenolysis Decrease gluconeogenesis Increase glycogen synthesis
159
What is released from pancreatic alpha cells
Glucagon
160
What is released from pancreatic beta cells
Insulin Proinsulin C-peptide Amylin
161
What is released from pancreatic delta cells
Somatostatin
162
What is released from pancreatic F cells
Pancreatic polypeptide
163
How much insulin is taken up by the liver
50%
164
Positive modulators of insulin secretion
``` ATP Beta agonists (G-alpha-s) Glucagon (G-alpha-s) CCK (G-alpha-q) ACh (G-alpha-q) ```
165
Negative modulators of insulin secretion
Somatostatin (G-alpha-i) Galanin (G-alpha-i) Alpha adrenergic agonists (G-alpha-i) Exercise
166
Oral Glucose Tolerance Test
Incretins, stimulated by oral glucose, enhance insulin release
167
Liver GLUT transporter
GLUT2
168
Muscle and adipose tissue GLUT transporter
GLUT4
169
What is the major stimulator of glucagon secretion
Amino acids
170
Glucagon GPCR
G-alpha-s
171
Somatostatin
Suppresses insulin, glucagon, and other hormones
172
Type I diabetes
Decrease insulin, preserved glucagon Ketoacids produced lead to metabolic acidosis Immune-mediated selective destruction of beta cells
173
Type II Diabetes
Resistant to action of insulin | Beta cells don't respond to increase in glucose
174
Thyroxine (T4)
``` Less active More abundant (90%) Half life = 8 days ```
175
Triiodothyronine (T3)
``` More active Less abundant (10%) Half life = 24 hours ```
176
Thyroid gland follicle
Follicular epithelial cell + Follicular lumen (colloid)
177
Thyroglobulin
Glycoprotein sequestered by follicular cells
178
TRH GPCR
G-alpha-q
179
TSH GPCR
G-alpha s
180
TSH stimulates
``` Iodide trapping Iodide oxidation Iodination Conjugation Endocytosis Proteolysis Secretion ```
181
Type 1 5'/3' deiodinases
Kidney Liver Thyroid Skeletal muscle
182
Type 2 5'/3' deiodinases
Pituitary CNS Placenta
183
Intracellular actions TH
Increase Na/K ATPase activity Stimulates mitochondria and respiratory enzymes Increase O2 consumption Increase metabolic rate Increase B-adrenergic receptor responsiveness
184
Extracellular and whole body response of TH (mainly catabolic)
``` Increase BMR Increase cardiac output Increase ventilation Increase food intake Increase gluconeogenesis/glycogenolysis Proteolysis > Proteogenesis Lipolysis > Lipogenesis ```
185
Hashimoto's thyroiditis
Antibodies against follicular cells and TSH receptors
186
Cretinism
Hypothyroidism during infancy
187
Cretinism symptoms
``` Mental retardation Short stature Delay in motor development Coarse hair Protuberant abdomen ```
188
Dwarfism
Develop hypothyroidism before fusion of growth plates
189
Grave's Disease
Autoimmune disorder
190
Cold nodules
Non-functioning | More likely to be malignant
191
Hot nodules
Functional adenomas or carcinoma
192
Pendrin defect
Iodide can't enter colloid, backflows into bloodstream
193
Propylthiouracil
Block deiodinases to assess T3 levels/sources
194
GHRH GPCR
G-alpha s
195
GH inhibitors
GH IGF-1 (directly: inhibits somatotrophs) IGF-1 (indirectly: inhibits GHRH release, stimulates somatostatin) Somatostatin
196
Growth hormone and prolactin
Same affinity for PRL receptor | PRL has no affinity for GH receptor
197
GH acute effects
Increased lipolysis Decreased glucose uptake Increases gluconeogenesis High doses => Insulin resistance
198
GH long term effects
Stimulate chondrocytes proliferation Promotes longitudinal bone growth Stimulates EC matrix formation Promotes growth in almost every cell of the body
199
Stimulators of GH release
``` Exercise Stress High protein meals Fasting Ghrelin ```
200
Ghrelin receptor
GH secretagogue receptor 1a (GHSR1a)
201
Inhibitors of GH release
Somatostatin Obesity Pregnancy Hyperglycemia
202
Somatostatin receptor
SSTR
203
IGF-1
Mediates somatic long-term effects of GH
204
When is IGF-1 highest
~12 years of age
205
When is IGF-2 highest
During fetal life
206
Other hormones that increase growth
Thyroid hormone Sex steroids Insulin
207
Other hormones that decrease growth
Glucocorticoids Lack of T3 IR defect
208
Hormones that regulate body mass
Insulin Glucocorticoid Adiponectin Leptin
209
Hormones that regulate linear growth
``` GH IGF-1 and IGF-2 Insulin TH Glucocorticoids Androgens Estrogens ```
210
Where in the brain do leptin and ghrelin act
Arcuate nucleus Anorexigenic neuron Orexigenic neuron
211
Gigantism
Excess GH before puberty
212
Acromegaly
Excess GH after puberty | Growth of bone width and vital organs
213
GH deficiency
Pituitary dwarfism | Laron's syndrome
214
Where is PTH made and stored
Chief cells of parathyroids
215
Stimulators of PTH
Low EC Ca | Low EC MG
216
Inhibitors of PTH
``` High EC Mg High vitamin D Prolonged low Mg High plasma Ca FG23 ```
217
PTH effects on kidney
Increases Ca reabsorption Decreases phosphate reabsorption Stimulates 1-alpha-hydroxlyase
218
PTH effects on GI
Increase Ca reabsorption | Increase phosphate reabsorption
219
Vitamin D effects
Stimulates Ca reabsorption Stimulates phosphate reabsorption (NaPi) Inhibits PTH gene expression Inhibits self
220
Vitamin D conversion in the skin
7-Dehydrocholesterol => Cholecalciferol (Vitamin D3)
221
Vitamin D conversion in the liver
Cholecalciferol (Vitamin D3) => 25-Hydroxycholecalciferol (25-OHD3)
222
Vitamin D conversion in the kidney
25-Hydroxycholecalciferol (25-OHD3) => 1,25-(OH)2D3
223
Calcitonin stimulators
High EC [Ca2+]
224
Calcitonin inhibitors
Low EC [Ca2+]
225
Effects of calcitonin
Inhibits osteoclasts and osteocytic osteolysis | G-alpha s in osteoclasts
226
Bone cells with PTH receptors
Osteoblasts only
227
What does pulsatile bone release lead to?
Bone formation
228
What does continuous PTH release lead to?
Bone resorption
229
Vitamin D direct effect
Stimulates osteoblasts to release M-CSF to mature osteoblasts Bone resorption
230
Vitamin D indirect effect
Increased P and Ca2+ from kidney and GI promotes bone mineralization
231
Osteocytic osteolysis
Transfer of Ca2+ from interior to bone surface
232
Role of OPG
Bind RANK ligand so it can't bind RANK | Inhibits osteoclast from doing its job
233
What does RANK ligand do
Increases differentiation and activity of osteoclasts
234
V-type proton pump
Acidifies lacuna, dissolves minerals, stimulates lysosomal enzymes
235
Integrins
Bind vitronectin; seal
236
Lysosomal enzymes
Hydrolyze matrix proteins
237
Lacuna
Resorption space
238
Puberty
Period of development of secondary sex characteristics
239
LH role in males
Testosterone synthesis
240
FSH role in males
Spermatogenesis
241
Inhibins in males
Inhibit FSH release
242
Estrogens in males
Inhibit FSH and GnRH release
243
Testosterone in males
Inhibits LH and GnRH release
244
Why can't sertoli cells produce testosteron
Missing 17 alpha hydroxylase
245
Why can't leydig cells produce estradiol
Missing P450 aromatase
246
Effects of testosterone
Differentiation of external and internal male genitalia Spermiogenesis Erythropoiesis
247
Testosterone clinical assessment
Pubertal growth spurt Deepening voice Increased muscle mass, growth of skeletal muscle Growth of hair
248
What does FSH promote in males
Androgen Binding Proteins P450 Aromatase Growth factors Inhibins
249
Growth factors in males
Support sperm cells, spermatogenesis, and stimulate leydig cells
250
Sperm volume in semen
10%
251
Seminal plasma volume in semen
90%
252
What supplies sperm its energy
Fructose
253
Male sex act sympathetic innervation
T1 to T12 | L1 to L3
254
Male sex act parasympathetic innervation
S2 to S4
255
Innervation responsible for erection
Parasympathetic
256
Innervation responsible for emission
Sympathetic
257
What causes ejaculation
Spinal cord reflex
258
Ovary cortex
Developing follicles Corpus lutea Stroma
259
Ovary medulla
Blood vessels and stromal elements
260
Menarche
Beginning of menstrual cycles
261
Thelarche
Breast development
262
Adrenarche
Increase in adrenal androgen secretion that occurs around the age of 6-8 years
263
LH receptors in women
Theca and granulosacells
264
FSH receptors in women
Granulosa cells
265
Luteal phase
Negative feedback by estrogen/progesterone
266
Follicular phase
Positive feedback by estrogen/progesterone
267
Why can't theca cells produce estrogen
lack aromatase
268
Why can't granulosa cells produce androgens?
Lack 17 alpha hydroxylase
269
Primordial follicles
Appear at 6 weeks in the fetus Complete set @ 6 months after birth Represents 95% of follicles
270
What hormone is dominant during follicular phase
FSH
271
Zona compacta and zona spongiosa
Functional layer of the endometrium
272
Zona basalis
Layer left behind after menstruation
273
Hormone levels during menopause
Ovarian steroid levels fall Gonadotropin levels rise High FSH, LH Low estrogen, progesterone, inhibin
274
Chromaffin cell
Modified postganglionic sympathetic neuron | Stimulated by pre-ganglionic acetylcholine
275
What blocks L-type Ca2+ channels in chromaffin cell
Nifedipine
276
What blocks N-type Ca2+ channels in chromaffin cell
Conotoxin GVIA
277
What blocks P/Q-type Ca2+ channels in chromaffin cell
Agatoxin IVA
278
P/Q type Ca2+ channgels
Elicits exocytosis by action potentials
279
L-type Ca2+ channels
Increases stimulus-secretion efficacy as frequency increases
280
Normal/Basal conditions Sympathetic tone
Low rate firing
281
Normal/Basal conditions catecholamine release
Modest
282
Normal/Basal conditions response
Maintain normal: - Blood pressure - Heart rate - Vascular tone - Enteric activity - Blood glucose level
283
Sympatho-adrenal stress reflex sympathetic tone
Increased | Burst mode firing
284
Sympatho-adrenal stress reflex catecholamine release
Max
285
Sympatho-adrenal stress reflex results
Increased: - Blood pressure - Cardiac output - Pulmonary ventilation - Blood flow to muscle - Glucagon secretion
286
Stress Reflex
Heightened splanchnic firing Nicotinic path desensitized PACAP released from splanchnic nerve
287
PAC1-R GPCR
G-alpha s | G-alpha q
288
PACAP and ACh
PACAP release in ACh independent
289
PKC role in PACAP signaling
Activates NCX Stimulate T-type Ca channels Gap junctions and allows for communication between cells
290
What does PACAP elicited catecholamine secretion need
``` Extracellular calcium PLC activity PKC activity NCX activity (depolarization) T-type Ca2+ channel activity ```
291
Carbon Fiber Electrode
Measures actual catecholamine release as a function of time (electrochemistry)
292
Patch Pipette
Measures current and capacitance
293
Fast scanning Cyclic Voltammetry
Detects Norepinephrine and Epinephrine
294
Electrical Methods used in determining mechanisms of secretion in chromaffin cells
Carbon Fiber electrode Patch Pipette Fast scanning cyclic voltammetry
295
Fast scanning cyclic voltammetry
Found that chromaffin cells release epinephrine only if they contain PNMT
296
PNMT
Converts norepinephrine to epinephrine
297
Physiological functions of cortisol
Increase blood glucose to supply energy Maintenance of cardiac contractility Immunosuppressive/anti-inflammatory
298
Regulation of cortisol levels
Diurnal variation in cortisol secretion
299
Assessing Serum cortisol
Timing Protein binding Episodic secretion
300
Basal secretory rate of cortisol
~9-12 mg per day
301
Stress response cortisol release
Secretory rate increases up to ~10x normal
302
Stimulation of Aldosterone production
Renin-Angiotension system Hyperkalemia ACTH
303
Physiological effects of aldosterone
Increases Na/H2O reabsorption | Increases K/H secretion
304
Target tissues of aldosterone
``` Kidney Sweat glands Salivary glands GI tract Muscle Bone ```
305
Cushing's Syndrome hormone levels
Elevated Cortisol Suppressed ACTH Suppressed CRH
306
Cushing's disease hormones
Elevated ACTH Elevated Cortisol Suppressed CRH
307
Ectopic ACTH hormones
Elevated cortisol levels Elevated ACTH Suppressed CRH
308
Dexamethasone test normal patient
Negative feedback decreases CRH, ACTH, and cortisol
309
Dexamethasone
Corticosteroid that mimics cortisol
310
Dexamethasone test adrenal tumor
No suppression of cortisol because the tumor itself is causing cortisol hyper-secretion
311
Dexamethasone test cushing's disease
No suppression of cortisol under low dose | Some suppression of cortisol at high dose
312
Dexamethasone test ectopic ACTH
No suppression of cortisol because ACTH is produced from ectopic tumor
313
Cushing's Screening
24-hour urinary free cortisol Very low dose dexamethasone Salivary cortisol
314
Cushing's Diagnostic
Low and high dose dexamethasone tests Measure plasma ACTH Imaging to look for tumor
315
Petrosal Sinus testing use
Ectopic ACTH vs Cushing's disease
316
Petrosal sinus testing interpretation
Petrosal/peripheral ACTH is >2:1 = Cushing's disease | Petrosal/peripheral ACTH is <2:1 = Ectopic ACTH
317
Primary adrenal insufficiency
Adrenal gland problem
318
Secondary adrenal insufficiency
Pituitary problem
319
Tertiary adrenal insufficiency
Hypothalamus problem
320
Adrenal insufficiency results
``` Decreased blood glucose Decreased lipolysis Decreased gluconeogenesis Lack of energy Muscular weakness Inability to handle stress ```
321
Primary adrenal insufficiency hormones
Low cortisol | High CRH and ACTH
322
Primary Adrenal insufficiency causes
``` Autoimmune Infection Cancer Adrenal hemorrhage Infiltrative disorders Congenital adrenal hyperplasia Drugs ```
323
ACTH stimulation test
Tests between primary and secondary adrenal insufficiency
324
ACTH stimulation test primary adrenal insufficiency
Low dose ACTH = no increase in cortisol | High dose ACTH = no increase in cortisol
325
ACTH stimulation test Secondary adrenal insufficiency
Low dose ACTH = no increase in cortisol | High dose ACTH = Cortisol will increase
326
Insulin tolerance test
Insulin induces hypoglycemia => Cortisol production increases => Glucose back to normal
327
Metyrapone teste
Inhibits 11-beta hydroxylase => 11-deoxycortisol accumulates and cortisol decreases => converted to 17-OH corticosteroid by liver => Excreted in urine
328
Primary hyperaldosteronism
Conn's disease
329
Conn's disease cause
adrenal tumor
330
Conn's disease hormones
Low Renin Low Ang II High Aldosterone
331
Conn's disease effects
Increased NaCl reabsorption Increased ECF volume Increased K secretion Metabolic alkalosis
332
Secondary hyperaldosteronism causes
``` Renal artery stenosis Congestive heart failure Renal salt wasting Juxtaglomerular hyperplasia Liver cirrhosis ```
333
Secondary hyperaldosteronism hormones
Increased renin = RAAS activation
334
Primary adrenal insufficiency
Adrenal gland problem
335
Secondary adrenal insufficiency
RAAS problem
336
Primary adrenal insufficiency example
Addison's disease
337
Addison's disease hormones
Low aldosterone = RAAS activation | High ACTH
338
Addison's disease causes
``` Autoimmune Infection Cancer Adrenal hemorrhage Infiltrative disorders Congenital adrenal hyperplasia ```
339
Pheochromocytoma symptoms
Sweating Palpitations Headache
340
Pheochromocytoma
Excess secretion of catecholamines
341
Metabolic Syndrome Diagnostic criteria
Central obesity: waist circumferency >102 cm or 40 inches (male), >88 cm or 35 inches (female) Dyslipidemia: TG >1.7 mM, 150mg/dL Dyslipidemia: HDL-C <40mg/dL (male), <50 mg/dL (female) Blood pressure > 130/85 mmHg (or hypertension medication) Fasting plasma glucose > 6.1 mM, 110 mg/dL (Must have 3)
342
Role of 11b-HSD1 in hepatocyte hypothesis
Decreased dietary magnesium induces metabolic changes in hepatocytes that favor obesity and promote the onset of metabolic syndrome and complications
343
Mg deficiency findings
Decreased hepatic Mg and ATP Decreased glucose uptake, and accumulation Increased G6P content being used by H6PD Increased NADPH production Increased cortisol production from cortisone Increased 11-beta-HSd1 expression Increased intrahepatic triglyceride content and liver steatosis Increased Nf-kB translocation Increased TNF-alpha expression Upregulation of gluconeogenic genes, cholesterol related genes, and FAs- related genes via PPAR-g/SREBP1c
344
GLUT1
Resting uptake in most cells
345
GLUT2
Liver Beta islet cells Kidney Enterocytes
346
GLUT3
Brain
347
GLUT4
Muscle Adipose tissue Stimulated by phosphorylated AMPK
348
GLUT5
Jejunum
349
SGLT1
Enterocytes and S3 | 2:1 Na:glucose
350
SGLT2
S1 and S2 in proximal tubule | 1:1 Na:glucose
351
What happens to urine/serum K, Ca, Pi, Mg during polyuria
Urine levels of each increase | Serum levels of each decrease
352
Type 1 diabetes symptoms
Polyuria, nocturia Polyphagia Fatigue Weight loss
353
Type 1 diabetes
Destruction of beta cells | Little to no endogenous production of insulin
354
Type 2 diabetes
Beta cells are capable of producing insulin but it's either insufficient amount or resistance is present
355
Type 1 diabetes onset
Sudden
356
Type 1 diabetes age of onset
Any age, mostly young
357
Type 1 diabetes body type
Thin or normal
358
Type 1 diabetes Ketoacidosis
Common
359
Type 1 diabetes autoantibodies
Usually present
360
Type 1 diabetes endogenous insulin secretion
Low or absent
361
Type 1 diabetes Identical twins
50%
362
Type 1 diabetes prevalence
Less common
363
Type 2 diabetes onset
Gradual
364
Type 2 diabetes age of onset
Mostly in adults
365
Type 2 diabetes body type
Often obese
366
Type 2 diabetes ketoacidosis
Rare
367
Type 2 diabetes Autoantibodies
Absent
368
Type 2 diabetes endogenous insulin secretion
Normal, decreased, or increased
369
Type 2 diabetes identical twins
90%
370
Type 2 diabetes Prevalence
90-95% of US diabetics
371
Type 2 diabetes symptoms
Polyphagia Fatigue Nocturia
372
Type 2 diabetes risk factors
``` Familial disposition Overweight >45 years of age Physically active <3 times/week Diet History of gestational diabetes Race/Ethnicity ```
373
Type 1 diabetes risk factors
Familial disposition Young age Viral infections Environment
374
Normal BMI
18.5-24.9
375
Overweight BMI
25-29.9
376
Obese BMI
30-39
377
Extremely obese BMI
40+
378
Normal HbA1C
4%-5.6%
379
Pre-diabetic HbA1C
5.7-6.5%
380
Diabetic HbA1C
6.6%
381
Normal glucose range
65-100 mg?dL | 3.5-5.5 mM
382
Pre-diabetic fasting glucose
>100 and <126
383
Pre-diabetic post prandial blood glucose
>140 and <200
384
Diabetic Fasting blood glucose
> 126
385
Diabetic coma glucose level
>600 mg/dL
386
Diabetic post-prandial or random blood glucose
>200
387
Amount of criteria needed
One with symptoms | Two without symptoms
388
Ultra-short-acting insulin
Aspart (novolog) Glulisine (apidra) Lispro (Humalog)
389
Intermediate-acting insulin
NPH | Used overnight, while fasting and between meals
390
Long-acting insulin
Detemir (Levemir) Glargine (Lantus) Used overnight, while fasting, and between meals
391
Treatment of Type 2 Diabetes
Sulfonyl-Urea Metformin Thiazolidinedione
392
Rate ADOPT study drugs most to least
Sulfonylurea Metformin Thiazolidinedione
393
Acute complications of diabetes
Hypoglycemia Diabetic Ketoacidosis (T1DM) Nonketotic hyperosmolar coma (T2DM)
394
Key features of DKA
``` Acetone/fruity breath Kussmaul respirations Dehydration Altered LOC Serum pH <7.3 Metabolic acidosis ```
395
Key features of Nonketotic hyperosmolar coma
``` Extreme dehydration Confusion Seizures Hypotension Tachycardia Serum pH > 7.3 Urine osmolarity >320 mOsm/L ```
396
Microvascular Chronic complications of diabetes
Retinopathy Nephropathy Neuropathy
397
Macrovascular Chronic complications of diabetes
Coronary artery disease Cerebrovascular disease Peripheral vascular disease
398
Nonvascular Chronic complications of diabetes
Gastroparesis Dermopathy Infections
399
Pre-eclampsia
Hypertension and proteinuria with onset after week 20 | Can have long-term sequelae affecting mother and fetus
400
Eclampsia
Convulsions or coma unrelated to other cerebral conditions with signs and symptoms of pre-eclampsia Can occur before or after birth
401
Most common symptoms of pre-eclampsia
``` Epigastric pain CNS involvement Nausea/vomiting Reduced platelets, elevated livere enzymes Pulmonary edema ```
402
Fetal outcomes of pre-eclampsia
``` Premature birth Intrauterine growth retardation Placental abruption Oligohydramnios Non-reassuring fetal surveillance ```
403
Pathophysiology of pre-eclampsia
``` Abnormal trophoblast invasion Poor spiral artery remodeling Placental ischemia Increased HIF1aa + placental oxidative stress Increased inflammatory cytokines Decreased anti-inflammatory cytokines Increased sFLT1, decreased PLGF and VEGF ```
404
Pre-eclampsia risk factors
``` Nulliparity Age >40 years Family history of pre-eclampsia Woman born small for gestational age Obesity/gestational diabetes Multi-fetal gestation Pre-eclampsia in previous pregnancy Poor outcome in previous pregnancy Fetal growth restriction, placenta abruption, fetal death Preexisting medical or genetic conditions ```
405
Mild pre-eclampsia blood pressure criteria
Systolic >140 and diastolic >90
406
Mild pre-eclampsia proteinuria criteria
300mg of proteinuria over 24 hours
407
Severe pre-eclampsia blood pressure criteria
Systolic >160 OR Diastolic >110
408
Severe pre-eclampsia proteinuria criteria
>5g in 24 hours
409
HELLP Syndrome diagnosis
Hemolysis Elevated liver enzymes Severe anemia unrelated to blood loss Low platelets
410
Hemolysis criteria HELLP
Two of these: Peripheral smear (schistocytes, burr cells) Serum bilirubin (>1/2 mg/dL) Low serum haptoglobin
411
Elevated liver enzymes criteria HELLP
AST or ALT > twice upper level of normal | Lactate dehydrogenase > twice upper level of normal
412
Low platelets criteria HELLP
<100,000/mm^3
413
Erectile Dysfunction definition
Inability of a man to achieve or maintain an erection sufficient for his or his partner's sexual needs
414
ED epidemiology
Experienced by >40% of men Atherosclerosis accounts for 50-60% of ED cases 35-50% of men with diabetes have ED
415
Prevertebral nerve plexuses for male sex act
Celiac 2 mesenteric 2 hypogastric
416
Ganglia of male sex act
Spermatic and pelvic
417
Physical causes of ED
``` Circulatory problems Nerve/heart disorders Diabetes Medications Smoking and alcohol use Prostate surgery Radiation Colon cancer surgery Neurological problems ```
418
Psychological causes of ED
Stress Depression Performance Anxiety
419
Diagnosis of ED
``` Duplex ultrasound Impulse to penile nerves to assess function Nocturnal penile tumescence Penile biothesiometry Dynamic infusion cavernosometry Corpus cavernosometry Magnetic resonance angiograpahy ```
420
Duplex ultrasound
Give prostaglandins => Should improve blood flow => stimulate erection
421
Tumescence
Engorgement of blood in erectile tissues due to decreased sympathetic tone
422
Nocturnal penile tumescence
If night time erections happen = psychological issue | If night time erections don't happen = non-psychological issue
423
Treatment options for ED
Lifestyle changes Medications Devices Surgery
424
Lifestyle changes ED
``` Exercise Balance dies Reduce/quit smoking and alcohol Lose weight Reduce stress/anxiety ```
425
Medications ED
Phosphodiesterase 5 inhibitors Prostaglandins Papaverine
426
Phosphodiesterase 5 inhibitors ED
PDE5 promotes breakdown of cGMP in penile vascular smooth muscle Inhibitors allow cGMP conentrations to remain high Sustained erection
427
Prostaglandins ED
Local injection | Transurethral cream
428
Papaverine ED
Local injection
429
Devices ED
Penis pump
430
Surgery ED
Prosthesis | Penile implant
431
Sildenafil brand names
Viagra | Revatio
432
Vardenafil brand names
Levitra | Staxyn
433
Taldalafil brand names
Cialis | Adcirca
434
Viagra side effects
``` Abnormal vision Constant headache Loss of hearing Facial flushing Nausea Chest pain Dizziness Pain during urination Nasal congestion ```
435
Sildenafil half life
3-4 hours
436
Vardenafil half life
4-5 hours
437
Tadalafil half life
17.5 hours
438
Endometriosis definition
Cells lining uterus appear and flourish outside of the uterine cavity, most commonly in the ovaries
439
Risk factors of endometriosis
Genetics Environment Aging
440
Why is endometriosis less common post-menopause?
Estrogen levels are lower post-menopause
441
Pathophysiology theories for endometriosis
Oxidative stress | Metabolic changes in endometrial tissue
442
Oxidative stress theory Endometriosis
8-iso-PGF2a and oxysterols promote oxidative stress
443
Metabolic changes in endometrial tissue theory Endometriosis
Increased adherence to peritoneal cells Dysregulation of matrix metalloproteinases Changes in VEGF-A, sVEGFR-1/2, angiopoietin-2, and IL-4 promoting vascularization
444
Theories on ectopic endometrial forrmation
Retrograde menstruation Mullerianosis Coelomic metaplasia Transplantation
445
Retrograde menstruation Endometriosis
Most common theory | Menstruation occurs in reverse direction
446
Mullerianosis Endometriosis
Cells with potential to become endometrial tissue are misplaced during embyronic development and organogenesis
447
Coelomic metaplasia Endometriosis
Coelomic epithelium is the common ancestor of endometrial and peritoneal cells
448
Transplantation Endometriosis
Endometriosis caused by abdominal incisional scars
449
Symptoms of Endometriosis
Pelvic pain Infertility Constipation Chronic fatigue
450
Pelvic pain Endometriosis
Dysmenorrhea Dyspareunia Dysuria
451
Dysmenorrhea
Painful menstrual cycle
452
Dyspareunia
Pain during sexual intercourse
453
Dysuria
Pain during urination
454
Endometriosis complications
``` Infertility Scarring Adhesion Pelvic cysts Chocolate cyst of the ovary Ruptured cyst Abscess Peritonitis Bowel obstruction ```
455
Endometriosis Diagnosis
Laparoscopic biopsy Ultrasound MRI
456
Stage 1 Endometriosis
Minimal | Findings restricted to only superficial lesions and possibly a few filmy adhesions
457
Stage 2 Endometriosis
Mild Some deep lesions are present in the cul-de-sac Plus Stage 1
458
Stage 3 Endometriosis
Moderate Presence of endometriomas on the ovary and more adhesions Plus stage 1 and 2
459
Stage 4 Endometriosis
Severe Large endometriomas, extensive adhesions Plus Stage 1, 2 and 3
460
Endometriosis Treatment options
Hormonal modification Other medications Surgery
461
Hormonal modification Endometriosis
``` Continuous GnRH Avoid xenoestrogens Contraceptive patches Aromatase inhibitors Danazol ```
462
Danazol
Suppressive steroid with androgen activity
463
Other medications Endometriosis
NSAIDs or morphine | Pentoxifylline
464
Pentoxifylline
PDE inhibitor to decrease cytokine production
465
Surgery Endometriosis
Conservative Semi-conservative Neurectomy
466
Conservative surgery Endometriosis
Cystectomy and adhesion resection
467
Semi-conservative surgery Endometriosis
Less invasive
468
Neurectomy surgery Endometriosis
More painful and serious cases
469
Vaginal childbirth and Endometriosis
Decreases recurrence
470
Caesarian section and Endometriosis
Increases recurrence
471
Somatic cell
Any cell in the body except sperm and egg cells
472
Sox9
Think males
473
Wnt4
Think females
474
What does SRY+ code for
TDF (testes determining factor)
475
When does spermatogenesis arrest
Primordial germ cell | Just before mitosis
476
When does oogenesis arrest
``` Prophase I (4n) of Meiosis I Metaphase II (2n) of Meiosis II ```
477
Meiosis regulation
Retinoic acid => promotes meiosis in females | Degraded in males => prevent meiosis
478
aneuploidy
Abnormal number of chromosomes
479
Spermiogenesis
Process by which spermatids become mature sperm
480
Spermiation
Heads of the spermatozoa are released from the Sertoli cell
481
Primordial follicles
Primary oocytes with a single layer of pre-granulosa cells | Complete set is made by 6 months after birth
482
What triggers ovulation
LH surge
483
What leads to resumption of meiosis I in females
Ovulation
484
What leads to resumption of meiosis II
Fertilization
485
Where does the nucleus come from during fertilization
Male and female contribute equally
486
Where does the cytoplasm come from during fertilization
Female
487
What is the trigger for reproduction
Puberty
488
Site of fertilization
Fallopian tubes
489
Cause of hCG release
Blastocyst cells release within a couple days after implantation has occured
490
hCG role
Keeps corpus luteum alive
491
Hatching
Degeneration of zona pellucida surrounding the blastocyst | Occurs 6-7 days after ovulation
492
Apposition
Blastocyst nears the endometrial lining
493
Adhesion
Blastocyst actually adheres to the endometrial lining
494
Invasion
Formation of syncytiotrophoblasts which take over maternal blood supply
495
Syncytiotrophoblast
Multi-nucleated cell of trophoblasts that have divided and fused
496
Lacuna
Blood lakes of maternal blood for nutrients
497
When does the placenta develop
14 days after fertilization
498
Hemochorial placenta
Maternal blood bathes chorionic villi
499
Molecular size to cross the placenta
500 MW
500
LH placental hormone
Chorionic Gonadotropin (CG) aka hCG
501
GH and prolactin placental hormone
Placental lactogen (PL)
502
ACTH placental hormone
ACTH-like protein
503
PTH placental hormone
PTH-related protein
504
GnRH, TRH, CRH, somatostatin placental hormone
Hypothalmic-like releasing hormones
505
Phasic contraction of uterus for birth
Tonic clamping to prevent hemorrhage
506
Progesterone in parturition
Quiescent, decreases uterine contraction
507
Estrogen in parturition
Promote uterine contraction | Primes uterus for labor
508
Prostaglandins & oxytocin in birth
Promote uterine contraction in labor
509
PRL role in lactation
Milk production
510
Oxytocin role in lactation
Milk ejection
511
Why doesn't lactation happen during pregnancy
Estrogen and progesterone are high and block PRL