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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
What does growth hormone signalling system promote rentenion of?
Promoting retention of calcium, phosphorus and nitrogen, necessary substrates for anabolism
26
What is type 1 diabetes?
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
27
What is type 2 diabetes?
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
28
4 types of cell of the pancrease
alpha cells, which produce glucagon; beta cells, which produce insulin; delta cells, which produce somatostatin; and PP cells, which produce pancreatic polypeptide.
29
How are pancreatic cells organised?
compact islets embedded within acinar tissue
30
How do alpha and beta cells regulate the usage of glucose?
production of glucagon and insulin, respectively.
31
Where does insulin get released from?
pancreatic beta cells
32
When does insulin get released?
when dietary carbohydrates or amino acids are abundant.
33
How does insulin stimulates the conversion of simple energy units?
by increasing glucose uptake in muscle and adipose tissue.
34
What is the sequence of the insulin protein?
2 peptide chains of 21 and 30 amino acids, linked by 2 disulphide bonds
35
What stimulates the conversion of active RAB-GTP into inactive RAB-GDP?
TBC1D4
36
What happens when TBC1D4 is inactivated by AKT phosphorylation?
allows active RAB to promote the movement of GLUT4 - containing vesicles to the cell surface.
37
Why is insulin administered by injection?
Insulin is destroyed in the GI tract
38
What is the elimination half life of insulin?
10 minutes
39
Where is insulin inctivated?
Inactivated in the liver and kidneys enzymically
40
What effect does renal impairment have on diabetes?
renal impairment lowers the insulin requirement
41
Why are there different types of insulin (rapid, short acting)?
Insulin formulations designed to avoid large fluctuations in plasma concentration
42
What is gestational diabetes?
occurs when your body can't make enough insulin during your pregnancy
43
How many people are affected by obesity in Europe and worldwide?
150 million people in Europe and 650 million people worldwide
44
What is type 2 diabetes caused by?
Caused by resistance to insulin in its target tissues such as skeletal muscle, liver and fat
45
What is an increased inicidence of type 2 diabetes linked to?
obesity epidemic
46
What does a HbA1c levels of less than 7% signify?
Mean plasma glucose of 8.3-8.9 mmol/l
47
What are factors used to determine optimal A1C targets?
The risk associated with hypoglycemia and other drug adverse effects, disease duration, life expectancy, relevant comorbidities, established vascular complications, patient attitude, resources
48
What is the frontline treatment for hyperhlycemia?
Metformin
49
What does an indulin sensitiser (metformin) do?
Increased insulin receptor expression
50
Side effects of metformin?
Diarrhea and nausea – Lactic acidosis, rare but potentially fatal – Contraindicated in renal, cardiac and hepatic insufficiency
51
What are metformin and phenformin synthetic derivative of?
Galegine
52
What is tissue specific effect of metformin (weight)?
Weight neutral
53
What function does metformin disturb?
Incretin function and the microbiome
54
Where does metformin act?
Liver
55
What is another name for SGLT2 inhibitors?
Glifozins
56
How much (g) does the kidney filter and reabsorb a day?
180g
57
What are responsible for reabsorption in the kidneys?
Sodium glucose cotransporters
58
Where are SGLT1/2 located?
Proximal tubule
59
What do SGLT2 inhibitors enhance?
SGLT2 inhibitors enhance glucose excretion, leading to a reduction in plasma glucose levels
60
What does SGLT2 inhibition result in?
reducing hyperglycaemia
61
Side effects of SGLT2 inhibitors?
Glucosuria increases risk of genitourinary infection – Potential for hypoglycaemia – Clinical trials into dapagliflozin showed an increased incidence of liver damage and some cancer
62
What is SGLT2 inhibitors contraindicated with?
patients with nephropathy
63
Tissue specific effects of SGLT2 inhibitors?
Weight loss
64
Where are incretin hormones produced and what do they enhance?
They are produced by the gut in response to food intake and have been demonstrated to enhance glucose-induced insulin secretion
65
What is GLP-1?
is a hormone secreted by the gut in response to food intake. and is an incretin hormone.
66
What are GLP-1 mimetics?
GLP-1 mimetics are a class of medications used to treat diabetes that act by mimicking the action of endogenous GLP-1.
67
What is an incretin mimetic?
Exanatide, a synthetic version of exendin-4, a peptide found in the saliva of the gila monster
68
What is an alternative to exanatide?
Liraglutide
69
How are incretin mimetics administered?
subcutaneously, twice daily, not degraded in the gut
70
What are incretin hormones used with?
In combination with metformin and a sulphonylurea in poorly controlled obese patients
71
Side effects of incretin hormones?
Hypoglycemia and gastrointestinal upset, rarely pancreatitis
72
What is an example of a DPP-IV inhibitor?
Sitaglipitin Phosphate
73
When is DPP-IV inhibitors used as monotherapy?
after failure of exercise and diet for glycemic control
74
When is DPP-IV inhibitors used as duotherapy?
Duo therapy with both TZDs or metformin
75
How is DPP-IV inhibitors adapted to renal disease?
Reduced
76
How does DPP-4 inhibitors affect the cardiovascular system?
Reduces cardiovascular complications and atherogenicity
77
Where do DPP-4 inhibitors act?
Pancrease
78
Examples of sulfonylureas?
Tolbutamide, Glibenclamide, Glipizide
79
Why is chlorpropamide note used?
Long duration of action can cause hypoglycemia – Has an anti diuretic hormone like effect that can cause hyponatremia
80
What do 2nd generation sulfonylureas demonstrate?
2nd Generation sulfonylureas demonstrate increased potency, but maximum hypoglycemic effect no better than tolbutamide
81
Where do sulphonylureas bind?
High affinity binding sites for sulphonylureas are found on the KATP channels of pancreatic b cells
82
What does binding of sulphonylureas cause in the cell?
Binding of sulphonylureas cause depolarisation and influx of Ca2+ resulting in insulin secretion
83
What are the side effects of sulphonylureas?
3% Suffer GI disturbance – Weight gain, allergy * Stimulate appetite – Hypoglycaemia!
84
What drugs are referred to as insulin secretagogues?
Sulfonylureas, meglitinides and glucagon-like peptide 1 receptor agonists (GLP-1RAs)
85
Where do insulin secretagogues act?
on pancreatic β cells to increase insulin secretion
86
Major side effects of insulin secretagogues?
Because they increased glucose uptake, their major side effects are hypoglycemia and weight gain
87
Why can Meglitinides/Sulfonylureas not be used in patients with renal disease?
concerns over clearence
88
What should the decision of what drug to use in duotherapy be based on?
presence or absence of known atherosclerotic CVD.
89
What class of drugs is metformin in?
Biguanides.
90
What do Thiazolidinediones do?
increase insulin sensitivity
91
What do GLP1RAs do?
augmenting glucose-stimulated insulin secretion, delay gastric emptying, decrease glucagon levels, and decrease food intake.
92
What are the major causes of morbidity of diabetes?
cardiovascular problems (60%) – Renal complications (10%) – Infection (6%)
93
How can the diabetic kidney become damaged?
– Glomerular injury – Ischemia – Infection
94
What is hypertrophy?
excessive development of an organ without an increase in cell number
95
What causes proteinuria at the level of the glomerulus?
both hemodynamic effects and injury to the individual components of the glomerular filtration barrier primarily lead to proteinuria
96
What contributes secondarily to proteinuria?
Mesangial cell injury
97
How can diabetic nephropathy progression be reduced?
Progression can be reduced by improved glycemic control and aggressive reduction of blood pressure
98
What drugs should be avoided in diabetic nephropathy?
Oral hypoglycemics that are excreted by the kidney should be avoided
99
When do Kimmelstiel-Wilson lesions appear?
Over diabetic nephropathy
100
What does angiotensin II cause?
direct vasoconstriction
101
What do ACE inhibitors block?
The enzyme that converts ATI to ATII
102
What peptide do ACE inhibitors interfere with?
ACE inhibitors also interfere with the degradation of bradykinin, a peptide that causes vasodilation
103
An example of Angiotensin II Receptor Antagonists
sartans
104
What are sartans and an example of the drug?
Non-peptide, orally active AT1 receptor antagonists, irbesartan

Drug action on body systems 2 (4 decks)

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