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Drug action on body systems 2 > MCQ 1 > Flashcards

MCQ 1 Flashcards

1
Q

What is a common side effect of insulin therapy in Type 1 diabetes?

A

acute, episodic hypoglycemia

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2
Q

What does long term use of ACE inhibitors for the management of hypertension cause?

A

hypoaldosteronism

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3
Q

What are 3 horomones releasd by the hypothalamus/ median eminence?

A

Dopamine (tyrosin derivative), growth-hormone releasing hormone, gonadotrophin-releasing hormone (GnRH)

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4
Q

What are 3 horomones releasd by the anterior pituitary?

A

Thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteniziing hormone (LH)

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5
Q

What are 2 horomones releasd by the posterior pituitary?

A

Vasopressin/ anrti-diuretic hormone, oxytocin

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6
Q

What are 2 horomones releasd by the thyroid?

A

Thyroxine, calcitonin

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7
Q

What are 2 horomones releasd by the adrenal cortex?

A

Aldosterone, cortisol

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8
Q

What are 2 horomones releasd by the adrenal medulla?

A

adrenaline, noradrenaline

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9
Q

What are 2 horomones releasd by the pancreas?

A

insulin, glucagon

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10
Q

Endocrinology definition

A

Endocrinology is the study of hormones and forms one of the body’s
major communication system

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11
Q

Hormone definition

A

A hormone is a chemical messenger, commonly distributed via the circulation, that elicits specific effects by binding to a receptor on or inside
target cells

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12
Q

Three major types of hormones

A

peptides, and the derivatives of amino acids and cholesterol

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13
Q

What regulates hormone production?

A

Negative and, occasionally, positive feedback, and cyclical mechanisms operate to regulate hormone production

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14
Q

How do clinical endocrine disorders arise?

A

Clinical endocrine disorders usually arise through too much, too little or disordered hormone production

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15
Q

What do disulphide bridges linke in the insulin receptor?

A

Link the alpha subunits of he insulin receptor to one another and to 2 identical beta subunits.

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16
Q

Where does insulin bind and what happens after binding?

A

Alpha subunits resulting in autophosphorylation of the intracellular domains of the beta subunits

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17
Q

How is the PI3 kinase pathway activated?

A

IRS1 or IRS2

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18
Q

What does Grb2 link?

A

IRS1 to the GDP/GTP exchange protein SoS

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19
Q

What triggers Ras?

A

Translocation of Grb2-SoS compLex triggers Ras by exchange of GTP for GDP

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20
Q

What is GH secretion stimulated by and where is it released into?

A

Its secretion is stimulated by GHRH, released into the portal
system from the hypothalamus.

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21
Q

What has inhibitory control over GH?

A

Somatostatin

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22
Q

Where does GH bind?

A

Liver

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23
Q

What does GH binding induce/

A

This induces an intracellular phosphorylation cascade involving the JAK/STAT (Janus kinase/signal transducing activators of transcription) pathway

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24
Q

Where are STAT proteins translocated from and what happens?

A

This induces an intracellular phosphorylation cascade involving the JAK/STAT (Janus kinase/signal transducing activators of transcription) pathway

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25
Q

What does growth hormone signalling system promote rentenion of?

A

Promoting retention of calcium, phosphorus and nitrogen, necessary substrates for anabolism

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26
Q

What is type 1 diabetes?

A

People who have type I
diabetes are unable to produce
the insulin signal. Has a juvenile onset, happens due to destruction of beta-cells, insulin-dependent

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27
Q

What is type 2 diabetes?

A

the cells of type II
diabetics have lost the ability to
respond to insulin. Has a maturity onset, happens due to defective insulin action, treatment by weight reduction and oral hypoglycaemic agents

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28
Q

4 types of cell of the pancrease

A

alpha cells, which produce glucagon; beta cells, which produce insulin; delta cells, which produce somatostatin; and PP cells, which produce pancreatic polypeptide.

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29
Q

How are pancreatic cells organised?

A

compact islets
embedded within acinar tissue

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30
Q

How do alpha and beta cells regulate the usage of glucose?

A

production of glucagon and insulin,
respectively.

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31
Q

Where does insulin get released from?

A

pancreatic beta cells

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32
Q

When does insulin get released?

A

when dietary
carbohydrates or amino acids
are abundant.

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33
Q

How does insulin stimulates the
conversion of simple energy
units?

A

by increasing
glucose uptake in muscle and
adipose tissue.

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34
Q

What is the sequence of the insulin protein?

A

2 peptide chains of
21 and 30 amino
acids, linked by 2
disulphide bonds

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35
Q

What stimulates
the conversion of active RAB-GTP into inactive RAB-GDP?

A

TBC1D4

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36
Q

What happens when TBC1D4 is inactivated by AKT phosphorylation?

A

allows active RAB
to promote the movement of GLUT4 - containing vesicles to the cell
surface.

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37
Q

Why is insulin administered by injection?

A

Insulin is destroyed in the GI
tract

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38
Q

What is the elimination half life of insulin?

A

10 minutes

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39
Q

Where is insulin inctivated?

A

Inactivated in the liver and
kidneys enzymically

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40
Q

What effect does renal impairment have on diabetes?

A

renal
impairment lowers the
insulin requirement

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41
Q

Why are there different types of insulin (rapid, short acting)?

A

Insulin formulations designed
to avoid large fluctuations in
plasma concentration

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42
Q

What is gestational diabetes?

A

occurs when your body can’t make enough insulin during your pregnancy

43
Q

How many people are affected by obesity in Europe and worldwide?

A

150 million people in Europe and 650
million people worldwide

44
Q

What is type 2 diabetes caused by?

A

Caused by resistance to
insulin in its target
tissues such as skeletal
muscle, liver and fat

45
Q

What is an increased inicidence of type 2 diabetes linked to?

A

obesity epidemic

46
Q

What does a HbA1c levels of less than 7% signify?

A

Mean plasma glucose of
8.3-8.9 mmol/l

47
Q

What are factors used to determine optimal A1C targets?

A

The risk associated with hypoglycemia and other drug adverse effects, disease duration, life expectancy, relevant comorbidities, established vascular complications, patient attitude, resources

48
Q

What is the frontline treatment for hyperhlycemia?

A

Metformin

49
Q

What does an indulin sensitiser (metformin) do?

A

Increased insulin receptor expression

50
Q

Side effects of metformin?

A

Diarrhea and nausea
– Lactic acidosis, rare but
potentially fatal
– Contraindicated in renal,
cardiac and hepatic
insufficiency

51
Q

What are metformin and phenformin synthetic derivative of?

A

Galegine

52
Q

What is tissue specific effect of metformin (weight)?

A

Weight neutral

53
Q

What function does metformin disturb?

A

Incretin function and the microbiome

54
Q

Where does metformin act?

A

Liver

55
Q

What is another name for SGLT2 inhibitors?

A

Glifozins

56
Q

How much (g) does the kidney filter and reabsorb a day?

A

180g

57
Q

What are responsible for reabsorption in the kidneys?

A

Sodium glucose cotransporters

58
Q

Where are SGLT1/2 located?

A

Proximal tubule

59
Q

What do SGLT2 inhibitors enhance?

A

SGLT2 inhibitors enhance
glucose excretion, leading to a
reduction in plasma glucose
levels

60
Q

What does SGLT2 inhibition result in?

A

reducing
hyperglycaemia

61
Q

Side effects of SGLT2 inhibitors?

A

Glucosuria increases risk of
genitourinary infection
– Potential for hypoglycaemia
– Clinical trials into
dapagliflozin showed an
increased incidence of liver
damage and some cancer

62
Q

What is SGLT2 inhibitors contraindicated with?

A

patients with
nephropathy

63
Q

Tissue specific effects of SGLT2 inhibitors?

A

Weight loss

64
Q

Where are incretin hormones produced and what do they enhance?

A

They are produced by
the gut in response to
food intake and have
been demonstrated to
enhance glucose-induced
insulin secretion

65
Q

What is GLP-1?

A

is a hormone secreted by the gut in response to food intake. and is an incretin hormone.

66
Q

What are GLP-1 mimetics?

A

GLP-1 mimetics are a class of medications used to treat diabetes that act by mimicking the action of endogenous GLP-1.

67
Q

What is an incretin mimetic?

A

Exanatide, a synthetic version of exendin-4, a peptide found in the
saliva of the gila monster

68
Q

What is an alternative to exanatide?

A

Liraglutide

69
Q

How are incretin mimetics administered?

A

subcutaneously, twice daily, not degraded in the gut

70
Q

What are incretin hormones used with?

A

In combination with metformin and a sulphonylurea in
poorly controlled obese patients

71
Q

Side effects of incretin hormones?

A

Hypoglycemia and gastrointestinal upset, rarely
pancreatitis

72
Q

What is an example of a DPP-IV inhibitor?

A

Sitaglipitin Phosphate

73
Q

When is DPP-IV inhibitors used as monotherapy?

A

after failure of
exercise and diet for glycemic
control

74
Q

When is DPP-IV inhibitors used as duotherapy?

A

Duo therapy with both TZDs or
metformin

75
Q

How is DPP-IV inhibitors adapted to renal disease?

A

Reduced

76
Q

How does DPP-4 inhibitors affect the cardiovascular system?

A

Reduces cardiovascular complications and atherogenicity

77
Q

Where do DPP-4 inhibitors act?

A

Pancrease

78
Q

Examples of sulfonylureas?

A

Tolbutamide,
Glibenclamide, Glipizide

79
Q

Why is chlorpropamide note used?

A

Long duration of action can
cause hypoglycemia
– Has an anti diuretic
hormone like effect that
can cause hyponatremia

80
Q

What do 2nd generation sulfonylureas demonstrate?

A

2nd Generation sulfonylureas
demonstrate increased
potency, but maximum
hypoglycemic effect no better
than tolbutamide

81
Q

Where do sulphonylureas bind?

A

High affinity binding sites for sulphonylureas are
found on the KATP channels of pancreatic b cells

82
Q

What does binding of sulphonylureas cause in the cell?

A

Binding of sulphonylureas cause depolarisation and
influx of Ca2+ resulting in insulin secretion

83
Q

What are the side effects of sulphonylureas?

A

3% Suffer GI disturbance
– Weight gain, allergy
* Stimulate appetite
– Hypoglycaemia!

84
Q

What drugs are referred to
as insulin secretagogues?

A

Sulfonylureas, meglitinides and glucagon-like peptide 1
receptor agonists (GLP-1RAs)

85
Q

Where do insulin secretagogues act?

A

on pancreatic β cells to
increase insulin secretion

86
Q

Major side effects of insulin secretagogues?

A

Because they increased glucose
uptake, their major side effects
are hypoglycemia and weight gain

87
Q

Why can Meglitinides/Sulfonylureas not
be used in patients with renal
disease?

A

concerns over
clearence

88
Q

What should the decision of what drug to use in duotherapy be based on?

A

presence or absence of known
atherosclerotic CVD.

89
Q

What class of drugs is metformin in?

A

Biguanides.

90
Q

What do Thiazolidinediones do?

A

increase insulin sensitivity

91
Q

What do GLP1RAs do?

A

augmenting glucose-stimulated insulin
secretion, delay gastric emptying, decrease glucagon
levels, and decrease food intake.

92
Q

What are the major causes of morbidity of diabetes?

A

cardiovascular problems
(60%)
– Renal complications (10%)
– Infection (6%)

93
Q

How can the diabetic kidney become damaged?

A

– Glomerular injury
– Ischemia
– Infection

94
Q

What is hypertrophy?

A

excessive development of an organ
without an increase in cell number

95
Q

What causes proteinuria at the level of the glomerulus?

A

both hemodynamic effects and
injury to the individual
components of the glomerular
filtration barrier primarily lead
to proteinuria

96
Q

What contributes secondarily to proteinuria?

A

Mesangial cell injury

97
Q

How can diabetic nephropathy progression be reduced?

A

Progression can be reduced by improved
glycemic control and aggressive
reduction of blood pressure

98
Q

What drugs should be avoided in diabetic nephropathy?

A

Oral hypoglycemics that are excreted by
the kidney should be avoided

99
Q

When do Kimmelstiel-Wilson lesions appear?

A

Over diabetic nephropathy

100
Q

What does angiotensin II cause?

A

direct
vasoconstriction

101
Q

What do ACE inhibitors block?

A

The enzyme that converts ATI to ATII

102
Q

What peptide do ACE inhibitors interfere with?

A

ACE inhibitors also interfere with the
degradation of bradykinin, a peptide that
causes vasodilation

103
Q

An example of Angiotensin II Receptor Antagonists

A

sartans

104
Q

What are sartans and an example of the drug?

A

Non-peptide, orally active AT1 receptor
antagonists, irbesartan

Drug action on body systems 2 (4 decks)

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