Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Systemic Pharma- Respiratory + Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

MoA of Incretins GLP-1 and GIP

A

Stimulated by food –> secreted from the GI tract –> increase β-cell proliferation (in the pancreas) -> increases insuline release –> increases cellular glucose uptake (in the liver & adipocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MoA of GLP-1 alone

A

stimulated by food –> released from the GI tract –> α-cell proliferation (in the pancreas) –> supresses glucagon secretion –> supressse glucose production (in the liver) –> Decreased hepatic glucose output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Actions of incretins are terminated by?

A

DPP-4 (dipeptidyl peptidase-4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diabetes mellitus is characterised by ——–

A

Hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type 1 diabetes vs Type 2

A

Type 1 Diabetes
* Absolute deficiency of insulin resulting from
autoimmune destruction of pancreatic β cells
* Insulin is essential for its treatment

Type 2 Diabetes (T2D)
* Insulin resistance
* Impaired insulin secretion
* Excess glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

1st line tx for DM type 1

A

Insulin (SC injection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

1st line tx for type 2 DM

A

Metformin (oral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CU of Insulin

A

Type 1 DM treatment
*SAFE IN GESTATIONAL DIABETES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is insulin not adm orally?

A

destroyed in the GI tract
(so we give it SC, IM ,IV)

* IV–> hyperglycemic emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do give pateints during a hyperglycemic emergency?

A

IV insulin
(used immediatly before the start of a meal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Short-acting insulin

A

lispro,
aspart,
glulisine

girls and lads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Adm of Short-acting insulin

A

Injected before a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Long-acting Insulin

A
  • neutral protamine hagedorn (NPH; insulin
    isophane);
  • glargine;
  • determir;
  • degludec

dani does great Nan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adm of Long-acting insulin

A

Dosage regimens may vary
* Multiple daily injections
* Rapid-acting analogues given with meals
* Basal insulin analogues injected once daily (often at night)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adm of Soluble insulin

A

IV emergency (diabetic ketoacidosis)–> Used immediately before the start of a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AE of insulin

A

HYPOGLYCAEMIA
* Weight gain
* Lipohypertrophy at injection site (change site of injection)
* Allergy and insulin resistance are rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MoA of Metformin

A

Activation of AMP-dependent protein kinase (AMPK) –> Reduces hepatic glucose production (gluconeogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

AE of Metformin

A
  • less likely to cause hypoglycaemia
  • weight loss
  • Dose-related gastrointestinal disturbances (e.g. anorexia, diarrhoea, nausea)
  • Lactic acidosis is rare but potentially fatal
  • Long-term use may interfere with absorption of vitamin B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Contraindications of Metformin

A

1) severe renal (excreted unchanged in urine) or hepatic disease,
2) hypoxic pulmonary disease,
3) shock or decompensated heart failure

why? causes Lactic acidosis (due to reduced drug elimination) which is fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CU of Metformin

A
  • T2D esp Obese patients
    (may promote weight loss and reduce Cardiovascular events and death)
  • Can be combined w/ other during in dual or triple therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

others drug calsses used in combo treatment of Diabtes (Esp type 2)

A

1) Sulfonylureas (1st/ 2nd gen)
2) Thiazolidinediones
3) GLP-1 mimetics
4) DPP-4 inhibitors
5) SGL T-2i

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

1st generation Sulfonylureas

A

Tolbutamide
Chlorpropamide (more sever AE, not used anymore)

-amide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Chlorpromaide vs Tolbutamide

A

Chlorpromaide -> longer-acting , can cause sever Hypoglycaemia
Tolbutamide –> shorter-acting, less sever AE

24
Q

AE of Chlorpropamide

A
  • Can cause sever hypoglycaemia
  • Flushing after alchohol(because of a disulfiram-like effect)
  • ADH action: hyponatraemia and water intoxication
25
Q

2nd generation Sulfonylureas

A

Glibenclamide (glyburide), glipizide,
glimepiride,
gliclazide

- 4 Gli’s

26
Q

which is more potent 1st gen or 2nd gen Sulfonylureas

A

2nd generation

27
Q

MoA of Sulfonylureas

A

Inhibit Katp channels on β-cells -> depolarization -> Ca+2 entery -> Insulin release

28
Q

AE of Sulfonylureas

A

1) Hypoglycemia
Can be severe and prolonged (Highest risk: chlorpropamide, glibenclamide, Low risk: tolbutamide)
2) Weight gain
3) GI upset less common
4) Allergic skin rashes and bone marrow toxicity
- Sulfonamide moiety

29
Q

Contraindications fo Sulfonylureas

A

PREGNANCY + Breastfeeding

  • Glyburide (and metformin) can be considered in pregnancy
30
Q

CU of Sulfonylureas

A

1) Early treatment of T2D
(Not useful in T1D or late-stage T2D–> Require functional B cells)
2) Can be used as Monotherapy if metformin is
contraindicated or not tolerated
3) Can be combined with other drugs in dual or
triple therapy

31
Q

Why are sulfonylureas not useful in T1D or late-stage T2D?

A

They Require functional B cells to work

32
Q

(drug) is superior in terms of CV disease prevention

A

Metformin

33
Q

Thiazolidinediones

A

aka GLITAZONES
Ciglitazone
troglitazone
Pioglitazone (only drug lisenced in Europe)

- not used anymore due to sever AE

34
Q

MoA of Glitazones (Thiazolinediones)

A
  • PPARγ-RXR Activation
  • Binds to DNA: transcription of several genes
  • Effects are slow in onset (1-2 months after start of treatment)
35
Q

Where are PPARγ found

A

adipose tissue, muscle and liver

36
Q

MoA of PPARγ in adipose tissue

A
  • Decreases plasma triglyceride levels
  • Increases lipogenesis and enhances uptake of fatty acids and glucose
  • Differentiation of adipocytes
37
Q

MoA of PPARγ in muscles and liver

A
  • Reduced hepatic glucose output
  • Increased glucose uptake into muscle
  • Enhanced effectiveness of endogenous insulin (insulin sensitizers): lowers exogenous insulin requirements
38
Q

AE of Thiazolidinediones (Glitazones)

A

1) Weight gain
2) Fluid retention
-Promotes Na+ reabsorption in collecting ducts
-Contraindicated in heart failure
3) Increased cardiovascular risk
4) Increased risk of fractures with chronic use
(Shunting of mesenchymal cells into adipocyte lineage and away of osteogenesis)
5) Other symptoms: headache, fatigue, GI disturbances

39
Q

Contraindications of Glitazones

A

1) HF –> due to fluid retention
2) Pregnancy
3) breastfeeding
4) children

40
Q

CU of Thiazolidinediones

A

* clincily not used anymore expect for Pioglitazone in EU

1) monotherapy when metformin is contraindicated
2) In additive with other oral hypoglycaemic drugs
3) may lessen the progression of impaired glucose tolerance in diabetes
4 May reduce the need for exogenous insulin in
T2D

41
Q

GLP1- Mimetics

A

Exenatide, liraglutide, duraglutide,
lixisenatide, semaglutide

-tide

42
Q

MoA of GLP-1 Mimetics (Exenatide, Liraglutadine, lixisenatide)

A

Mimic effects of GLP-1: longer acting
1) Increase insulin secretion
2) Suppress glucagon secretion
3) Slow gastric emptying
4) Reduce food intake (by an effect on satiety)
-Associated with modest weight loss

43
Q

Adm of GLP-1 mimetics

A

SC administration
- Administered before the first and last meal of the day
- Modified Release (MR) formulation: once weekly
injections

44
Q

AE of GLP-1 mimetics

A

1) Hypoglycaemia
2) GI effects
3) Pancreatitis is a rare but sometimes severe problem
4) weight loss

45
Q

CU fo GLP-1 mimetics

A

1) In T2D, in combination with other drugs when inadequate
2) Recommended in patients with atherosclerotic
cardiovascular disease, high cardiovascular risk,
kidney disease or heart failure (in addition to
metformin)
-Cardiovascular benefits
3) Recommended in obese patients, who have
failed on dual therapy

46
Q

DPP-4 inhibitors

A

sitagliptin,
vildagliptin,
saxagliptin,
linagliptin

47
Q

MoA of DPP-4 inhibitors

A

Competitively inhibit DPP-4
–> Potentiate endogenous incretins (GLP-1 and GIP)

48
Q

Adm of DPP-4 inhibitors (-agliptin)

A

oral

49
Q

AE of DPP-4 inhibitors (-agliptin)

A

Generally well-tolerated
* Less propensity for hypoglycaemia
* GI side effects
Less common but potentially serious:
* Occasional liver disease
* Worsening of heart failure (peripheral oedema)
* Pancreatitis

50
Q

CU fo DPP-4 inhibitors

A
  • Combination therapy with metformin (and/or other antihyperglycaemic agents) if blood glucose is not adequately controlled
  • As monotherapy if metformin is contraindicated or not tolerated
51
Q

Sodium-Glucose Co-Transporter 2 inhibitors (SGLT 2-i)

A

Canagliflozin,
dapagliflozin,
empagliflozin

52
Q

MoA of SGLT 2-i

A

Block SGLT-2 in proximal tubule
* Increased glucose excretion
* Increased osmotic natriuresis
- Decrease in weight and blood pressure
- Reduced preload
- Reduced intra-glomerular pressure

53
Q

SGLT-2i have benefits in?

A

Benefits in renal and CV outcomes in CKD, HF

*CKD: chronic kideny disease

54
Q

AE of SGLT-2i

A

1) Polyuria
2) UTIs
3) Vaginal yeast infections
4) Hyperkalaemia
5) Volume depletion (orthostatic hypotension)

* uti and infection because glucose in urine

55
Q

CU of SGLT-2i

A

1) T2D, usually in combination with other anti-diabetic drugs (e.g. metformin, insulin)
2) Monotherapy if metformin is not tolerated
3) Recommended in patients with atherosclerotic cardiovascular disease, high cardiovascular risk, kidney disease or HF (in addition to metformin)
3) Symptomatic chronic HF with reduced ejection fraction, inadequately controlled with a β-blocker, ACEI/ARB, and an aldosterone antagonist
4) CKD with albuminuria, alongside an ACEI/ARB

56
Q

Diabetes Management

A
  • Use of metformin as the optimal first-line drug unless contraindicated
  • After metformin, the use of 1 or 2 additional oral or injectable agents, with a goal of minimizing adverse effects if possible
  • A major focus on comprehensive cardiovascular risk reduction

Systemic Pharma- Respiratory + Endocrine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions