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Semester 1 > Exam 3 csv > Flashcards

Exam 3 csv Flashcards

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
Q

cGMP

A

a second messenger which activates dependent kinases or enzymes that produce AMP and Nitric Oxide

26
Q

Function of Nitric acid

A

Relaxes vascular smooth muscle. Example Viagra which breaks down cGMP causing relaxation of SM

27
Q

MOA of Steroid hormones

A

Activates transcription thus protein synthesis

28
Q

Once in the cytoplasm what happens to a steroid?

A

It binds to the nuclear hormone receptor (NHR).

29
Q

What are the 2 regions on NRH

A

Ligand/hormone binding domain and DNA binding domain.

30
Q

Ligand Binding domain

A

The mouth portion of the NHR that binds to the hormone

31
Q

DNA binding domain

A

The square portion that can binid onto the Hormone Response Elements

32
Q

Formation of the Anterior Pituitary

A

Derived from epithelial tissue that migrated from the mouth

33
Q

Formation of the Posterior Pituitary

A

Fromed by down growth of the brain

34
Q

Posterior Pituitary is controlled by?

A

The Hypothalamus

35
Q

What does the hypothalamus send to the PP

A

ADH and Oxytocin via the Hypothalamal hypophyseal

36
Q

What are the three 2nd messenger molecules

A

cAMP cGMP and Ca++

37
Q

Steroids are lipid soloble or water suluble?

A

Lipid Soluble

38
Q

auses on nonimune DM1

A

Secondary to diseases such as pancreatitis

39
Q

Cause of immune DM1

A

Damage to the Beta cells by the immune system

40
Q

C peptide in the blood is an indicator of what?

A

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
Q

Clinical manifestations of DM1

A

Hyperglycemia. Polydipsia. Polyurea. Polyphagia. Weightloss. Fatigue. Ketoacidosis

42
Q

Which drugs can cause endogenous insulin secretion

A

Sulfonureas

43
Q

3 major effects of DKA

A

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
Q

Prediabetes. HbA1C, Overnight fast and OGTT

A

HbA1c between 5.7 and 6.4. Overnight fast 100-125 and 2 hrs past OGTT of 140-199

45
Q

How does Obesity lead to DM2

A

Adipocytes release inflammatory cytokines that decrease the activity of gerlin in the GI tract which increases insulin resistance

46
Q

cells that use the polyol pathway

A

kidney. RBC’s. blood vessels. Eye lens. Nerves

47
Q

What are the 2 colplications associated with the polyol pathway (aldose reductase)

A
  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
Q

Complications associated with protein kinase C

A

can be inapropriately activated with hyperglycemia. Increase in DAG which activates PKC

49
Q

Clinical manifestations of the aldose reductase pathway

A

Cataracts and decreased NS AP’s

50
Q

Clinicl manifetsations of PKC pathway

A

Increased extracellular matrix. microvasular contractility. Microvascular permeability. Proliferation of endothelial and smooth muscle cells

51
Q

Clinical traits of Metabolic Syndrome (Syndrome X)

A

Big waist > 40”. Plasma Tryglycerides > 150. LDL > 40 male >50 female. PB > 138/85. Fasting Glucose > 100 and insulin resistance

52
Q

Diseases of the Adrenal Cortex

A

Addison’s. Cushing’s. Conn’s

53
Q

Cushing’s disease

A

Hyper secretion of ACTH from the AP

54
Q

Chushing’s sydrome

A

Excessive cortisol levels reguardless of the cause

55
Q

Causese of Cushing’s syndrome

A
  1. Iatrogenic from corticosteroids 2. ACTH secreting tumors
56
Q

Causes of Conn’s Disease

A

Excessive aldosterone secretion by the adrenal cortex

57
Q

Physiology of Conn’s disease

A

Hyper aldosteronism lading to increase in Na and H2O reabsrbtion and elimination of K

58
Q

Cause of addisions disease

A

Destruction of the adrenal cortex leading to a decrease in cortisol and mineralcorticoids

59
Q

Clinical manifestations of addisons

A

Weakness. Adnorexia. Weightloss. tan skin. hypotension

60
Q

Causes of phenochromocytosis

A

hypersecretion of catecholamines because of a tumor on the adrenal medula

61
Q

Manifestations of phenochromocytosis

A

HTN. Tachycardia. Dysrhythmia. Diaphoresis. Headache

Semester 1 (15 decks)

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