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Semester 1 > Exam 3 csv > Flashcards

Exam 3 csv Flashcards

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1
Q

What are the functions of target cell receptor hormones?

A

Recognize and bind to particular hormone and Initiate a signal to intracellular effectors

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2
Q

Sensitivity of the target cell is relatred to what?

A

The number of receptors on the target cell

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3
Q

What does estrogen do during pregnancy related to receptors?

A

It stimulates the production of more oxytocin receptors

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4
Q

Priming up (Up regulation)

A

Increase the number of receptors on target cells

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5
Q

Desensitization ( Down Regulation)

A

Decrease the number of receptors on the target cells

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6
Q

Example of Desensitization

A

In non insulin dependent Diabetes it is thought that the number of insulin receptors is reduced.

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7
Q

Snergistic Hormonal Interactions

A

Two hormones work together to produce a result. Example Vitamin D and PTH

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8
Q

Additive Hormonal Interactions

A

Each hormone separately produces a response together they stimulate a greater response. Example Epi and NE work together in mass activation of the sympatheric NS

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9
Q

Complementary Hormonal Interactons

A

Each hormone stimulates different steps in the process. Example, In Spermatogenisis FSH and testosterone stimulate different steps in the process.

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10
Q

Permissive Hormonal Interactions Effects

A

Hormome enhances the responseivness of a target organ to a second hormone . Example during menstration the increase in of estrogen induces the formation of more receptors for progesterone

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11
Q

AntagonisticHormonal interaction Effects

A

Action of one hormone antagonizes the effects of another. Example Insulin and Glucagon

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12
Q

4 types of cellular surface messengers

A

G- Protein linked- Ion channel Receptors- Tyrosine Kinase Linked Receptors- Receptors with intrinsic enzyme activity

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13
Q

What are signal transduction mechanisms

A

Hormones that use a 2nd messenger system

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14
Q

Examples of hormones that use the G protein system

A

Chatecolomines such as Epi and NE

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15
Q

What happens when Epi or NE bind to a receptor

A

G protein dissociates ond one portion moves to activate the adenylate clyclase. This causes the breakdown of ATP into cAMP and 2 inorganic phosphates (Ppi). cAMP activates protein Kinase. Kinase phosphoralates (attaches) phosphate groups to different enzymes. This alters the metabolism of the cell.

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16
Q

Wha inactivates cAMP

A

Phosphodiesterase

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17
Q

Clinical example of cAMP activation.

A

Theopholin is used to raise cAMP levels in bronchial smoothe muscle. Thus dilates the bronchials.

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18
Q

Action of second messenger Phospholipase C

A

catalyzes the formation of IP3 and DAG

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19
Q

Sequence of events for Phospholipase C

A
  1. Hormone binds to the receptor 2. Activation of Phospholipase C 3. Formation of IP3 and DAG. 4 IP3 diffuses through the ctoplasm to the ER. 5. In the ER stimulation and release of Ca++ 6. Ca++ binds to calmodulin
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20
Q

Functions of calmodulin

A

Activates a number of kinase enzymes. Alters the metabolism of the cell Example. Ca++/ Calmoduiln complex in smooth muscles causes contraction

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21
Q

Function of DAG

A

Activates protein kinase C and activates or deactivates other proteins or enzymes

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22
Q

Example of DAG

A

Breakdown of glycogen into glucose in the river

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23
Q

Function of Tyrosine Kinase

A

Causes the cell to produce GLUT-4 and activation of MAP

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24
Q

GLUT-4

A

A transporter which allows glucose to enter the cell. Glucose can then be stored as glycogen or broken down into pyruvic acid and utilized in the Kreb’s cycle

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25
cGMP
a second messenger which activates dependent kinases or enzymes that produce AMP and Nitric Oxide
26
Function of Nitric acid
Relaxes vascular smooth muscle. Example Viagra which breaks down cGMP causing relaxation of SM
27
MOA of Steroid hormones
Activates transcription thus protein synthesis
28
Once in the cytoplasm what happens to a steroid?
It binds to the nuclear hormone receptor (NHR).
29
What are the 2 regions on NRH
Ligand/hormone binding domain and DNA binding domain.
30
Ligand Binding domain
The mouth portion of the NHR that binds to the hormone
31
DNA binding domain
The square portion that can binid onto the Hormone Response Elements
32
Formation of the Anterior Pituitary
Derived from epithelial tissue that migrated from the mouth
33
Formation of the Posterior Pituitary
Fromed by down growth of the brain
34
Posterior Pituitary is controlled by?
The Hypothalamus
35
What does the hypothalamus send to the PP
ADH and Oxytocin via the Hypothalamal hypophyseal
36
What are the three 2nd messenger molecules
cAMP cGMP and Ca++
37
Steroids are lipid soloble or water suluble?
Lipid Soluble
38
auses on nonimune DM1
Secondary to diseases such as pancreatitis
39
Cause of immune DM1
Damage to the Beta cells by the immune system
40
C peptide in the blood is an indicator of what?
Insulin synthesis. A and B peptide form insulin from pre proinsulin when C peptide is cleaved off in the Golgi apparatus of the Beta cell
41
Clinical manifestations of DM1
Hyperglycemia. Polydipsia. Polyurea. Polyphagia. Weightloss. Fatigue. Ketoacidosis
42
Which drugs can cause endogenous insulin secretion
Sulfonureas
43
3 major effects of DKA
Profound loss of insulin leads to increase in glucose. Stress from DKA activates NE and Epi which surpress insulin production further leading it increase in glucose and Hyperosmolar urine pulls water from circulation leading to hypervolemic shock.
44
Prediabetes. HbA1C, Overnight fast and OGTT
HbA1c between 5.7 and 6.4. Overnight fast 100-125 and 2 hrs past OGTT of 140-199
45
How does Obesity lead to DM2
Adipocytes release inflammatory cytokines that decrease the activity of gerlin in the GI tract which increases insulin resistance
46
cells that use the polyol pathway
kidney. RBC's. blood vessels. Eye lens. Nerves
47
What are the 2 colplications associated with the polyol pathway (aldose reductase)
1. Increase in sorbitol causing water to diffuse into the cells (vision changes.a damages Schwann cells. RBC's become swollen and stiff. 2. Reduction in glutathione leading to oxidation injury particularly in blood vessels
48
Complications associated with protein kinase C
can be inapropriately activated with hyperglycemia. Increase in DAG which activates PKC
49
Clinical manifestations of the aldose reductase pathway
Cataracts and decreased NS AP's
50
Clinicl manifetsations of PKC pathway
Increased extracellular matrix. microvasular contractility. Microvascular permeability. Proliferation of endothelial and smooth muscle cells
51
Clinical traits of Metabolic Syndrome (Syndrome X)
Big waist > 40". Plasma Tryglycerides > 150. LDL > 40 male >50 female. PB > 138/85. Fasting Glucose > 100 and insulin resistance
52
Diseases of the Adrenal Cortex
Addison's. Cushing's. Conn's
53
Cushing's disease
Hyper secretion of ACTH from the AP
54
Chushing's sydrome
Excessive cortisol levels reguardless of the cause
55
Causese of Cushing's syndrome
1. Iatrogenic from corticosteroids 2. ACTH secreting tumors
56
Causes of Conn's Disease
Excessive aldosterone secretion by the adrenal cortex
57
Physiology of Conn's disease
Hyper aldosteronism lading to increase in Na and H2O reabsrbtion and elimination of K
58
Cause of addisions disease
Destruction of the adrenal cortex leading to a decrease in cortisol and mineralcorticoids
59
Clinical manifestations of addisons
Weakness. Adnorexia. Weightloss. tan skin. hypotension
60
Causes of phenochromocytosis
hypersecretion of catecholamines because of a tumor on the adrenal medula
61
Manifestations of phenochromocytosis
HTN. Tachycardia. Dysrhythmia. Diaphoresis. Headache

Semester 1 (15 decks)

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