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Flashcards in Exam 3 csv Deck (61):
1

What are the functions of target cell receptor hormones?

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

2

Sensitivity of the target cell is relatred to what?

The number of receptors on the target cell

3

What does estrogen do during pregnancy related to receptors?

It stimulates the production of more oxytocin receptors

4

Priming up (Up regulation)

Increase the number of receptors on target cells

5

Desensitization ( Down Regulation)

Decrease the number of receptors on the target cells

6

Example of Desensitization

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

7

Snergistic Hormonal Interactions

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

8

Additive Hormonal Interactions

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

9

Complementary Hormonal Interactons

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

10

Permissive Hormonal Interactions Effects

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

11

AntagonisticHormonal interaction Effects

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

12

4 types of cellular surface messengers

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

13

What are signal transduction mechanisms

Hormones that use a 2nd messenger system

14

Examples of hormones that use the G protein system

Chatecolomines such as Epi and NE

15

What happens when Epi or NE bind to a receptor

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.

16

Wha inactivates cAMP

Phosphodiesterase

17

Clinical example of cAMP activation.

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

18

Action of second messenger Phospholipase C

catalyzes the formation of IP3 and DAG

19

Sequence of events for Phospholipase C

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

20

Functions of calmodulin

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

21

Function of DAG

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

22

Example of DAG

Breakdown of glycogen into glucose in the river

23

Function of Tyrosine Kinase

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

24

GLUT-4

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

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