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LAST TEST!!! > L91- Pharm Diabetes > Flashcards

L91- Pharm Diabetes Flashcards

1
Q

Discuss the structure and actions of the Insulin REceptor?

A

Heterodimer w/ Alpha and Beta Subunits

Alpha - binds insulin

Beta - Tyrosine Kinase domain

Tetramer formation as they come together and 2 beta subunits phopshorylate eachother producing a cascade that signa;s IRS and results in GLUT4 glucose transporters traveling from sequestered sites to cell surface …and transcription of other things like Glucokinase

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2
Q

Which Glucose transportrers are found where?

A

Glut 1 - in the brain always and doesn’t need insuline for transport of glucose

GLUT2 reulgates insulin release in response to blood glucose

Glut4 - inserted into membrane in muscles and adipose cells from intracellular storage vesicles in response to insulin

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3
Q

IS it more efficent to store energy as fat or glycogen in muscles?

A

Fat TG bc glycogen needs H2O for storage vs fat does not

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4
Q

How long does reuglar insulin act?

A

1 hour

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5
Q

How many ppm does insulin need to be to be “purified” in instances of allergenciity?

A

<10ppm then purified

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6
Q

What are the Ultra-Short acting insulins? How do they work?

A

Lispro, Aspart, Glulisine

Remain in monomer form in vial and don’t form hexamers so immediate use and peak at 15 minutes

take right before meals

(regular insulin forms hexamers in vials and so inject it and have to dilute it in tissues to work so 30 minute lag)

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7
Q

What are the long acting insulins? What’s differences between them?

A

Glargine and Detemir

Glargine - Beta insulin supplement that is 18-24 hours long lasting and no discrete peak

Detemir - goes into blood and binds serum albumin and slowly released from albumin; slight peak ~12 hours and lasts 18 hours

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8
Q

What are the different insulin delivery systems?

A

Insulin is a peptide and so will be degraded orally so has to be given enterally

POrtable Pen injectors

Continuous SQ insulin infusion device aka pumps - preffered in kids and recomended for people with difficulty obtaining target control - lower total insulin dose

Inhaled - Afrezza

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9
Q

What are the problems/contraindications in Inhaled insulins?

A

Short term release

CONTRAINDICATION in patients w/ chronic lung disease - smokers, COPD, ASthma

Problem if taking and get URI

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10
Q

Complications of Insulin therapY?

A

Hypoglycemia- TX is sugar/IV glucose

Allergy

Lipodystrophy at injection site –> hypertrophy of Sq fat tissue from multiple injections at same site and liposuction corrects this

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11
Q

What are the different classes of oral antidiabetic drugs?

A

Insulin secretagogies - Sulfonylureas or Meglitinides

Biguanides

Thiazolinediones

Alpha-glucosidase inhibtors

Glucagon-like polypeptide 1 (GLP1) Agonsistss

DDP4 Inhibitors

SGLT2 Inhibitors

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12
Q

Sulfonylureas - mechanism of action, Important considerations, what drgs are they?

A

Second Generation - fewer side effects and less drug interactions but more potent so more likely to produce hypoglycemia - Glyburide, Glipizide, Glimepiride vs First generations - tolbutamide, chlorpropamide, tolazamide, acetohexamide

Mechanism: insulin release from beta cells independent of glucose!!! Activate SUR1 receptor assocaited w/ K6.2 channel

Condiseration: Pt needs functioning beta cells to make and release insulin

HYPOGLYCEMIA!

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13
Q

What are the Meglitinides? Mechanism? Cautions? Indications?

A

Repalinide (Prandin)

Mechanism: modulate beta cell insulin release, same site of action as Sulfonylureas but weaker affinity for receptors - shorter action

CAUTION - metebolized by liver so careful in pts w/ hepatic impairment

NO SULFER STRUCTURE - good for patients allergic to sulfonylureas!

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14
Q

What drug is a “Biguanide”? Mechanism of action? Uses?

A

METFORMIN!!!

Blood glucose lowering ability not dependent on function beta cells - Euglycemic

Mechanism - not completely known but increases insulin sensitivity of tissues and reduces insulin resistance, stimulates glycolysis in tissues, reduces hepatic gluconeogenesis, slows GI glucose absorption w/ increased glucose to lactate conversion, reduction in Glucagon levels

FIRSTLINE TREATMENT FOR T2DM

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15
Q

What are the side effects of metformin?

A

GI!! Anorexia, N/V, abdominal discomfort and diarrhea

Usually transient at begining of therapy

Absorption of B12 impaired!!!!

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16
Q

What are contraindicatios for Metformin?

A

Renal or Hepatic disease

Alcoholism or conditions predisposing to tissue anorexia (like chronic cardiopulmonary dysfunction)

Increased Risk of Lactic Acidosis induced by Biguanides!!!

17
Q

What are other uses for Metformin?

A

Pts w/ refractory obesity

DB Prevention in PREDIABETES - obese middle aged person w/ impaired glucose tolerance

PCOS - can lead to reversal of anovulation

Gestational Diabetes- more effective in preventing hypoglycemia but higher changes of pre-term birth (compared to insulin)

Cancer - reduced risk of pancreatic cancer and used in cancer treatment (esp breast cancer)

18
Q

What are the Thiazolidinediones? How do they work? Use? Side Effects/ problems?

A

Rosiglitazone and Plioglitazone - enhance target tissue insulin sensitivity

Mechanism: activation of genes of PPAR-gamma (genes of lipid and glucose metab - peroxisome proliferator activated receptor)

PPAR-gamma is TF to increase things for glucose uptake and metab in muscle and adipose

Problems/Side EFfectS:

  • weght gain and redistribution from visceral fat to Subq sites
  • delayed effects from upregulating genes
  • BLADDER CANCER
  • P450 interactions
19
Q

What are the Alpha-glucosidase inhibitors? How do they work/mechanism of action? side effects?

A

Acarbose and Miglitol - Prevent GI breakdown of starches into monosaccharides and so less sugars absorbed in GI

Mechnaism- competitive inhibition of Alpha-Glucosidase so reduction in post-prandial glucose levels

Side Effects: FARTS!!! diarrhea, abdominal pain bc unabsorbed carbs get fermented in colon

Contraindicated in IBD!

Don’t work overtime bc ileum and colon can upreulgate glycosidases

20
Q

Problem w/ taking Acarbose/Miglitol w/ other Anti-DB agents?

A

Taking sulfonylureas or Insulins can cause patients to get hypoglycemic and if they are also on Alpha-glucosidase inhibitors then can NOT give patient sucrose bc can’t break it down so need to give Fructose/Glucose

21
Q

What are the Incretin based therapies?

A

Incretins are GI hormones that regulate blood glucose along with insulin and include Glucagon-like-peptide 1 (GLP1)

They sensitize the pancrease to glucose and suppress post-prandial glucagon release - INCREASE INSULIN RELEASE

Slow gastric emptying and increase satieity - weight loss

Only for T2DM bc require endogenous insulin

FX: cause insulin release so can see hypoglycemia

22
Q

the GLP-1 Agonists - how do they work? What are they?

A

T2DM - see reduction in post-prandial rise in GLP1

Synthetic GLP1 has different Alanine at 2 position so not broken down by DPP4 as quickly

Exenatide and Liraglutide

  • improve glucose control and cause weight loss
23
Q

What are the DDP inhibitors and how do they work

A

Block DDP4 degratation of endogenous incretin hormones (GLP1) which increase circulating levels of endogenous incretin to increase glucose mediated insulin secretion and decreased glucagon levels

Sitagliptic, Saxagliptin, Vildagliptin

24
Q

What are the SGLT2 Inhibitors? restrictions/side effects? Mechanism?

A

SGLT2 inhibitors block reabsorption of glucose by the kidney and so more excretion of glucose

Side effects: osmotic diuresis and dehydration, rapid weight loss, tiredness, worse UTIs

REstrictions: Severe renal imairment or diabetics w/ increased ketones or CV risk

Invokana / Canaglifozin and Farxiga / Dapaglifozin

25
Q

What is glucagon? Where is it made? What does it do? Affects?

A

Glucagon - Hyperglycemic hormone made by alpha cells and degrades by liver and kidney w/ short half life in blood

EFFECTS:

  • Metabolic: binds receptors in liver cells –> increass cAMP –> catabolism of glycogen and increased gluconeogenesis and ketogenesis –> increase blood glucose at expsence of hepatic glycogen
  • Cardiac: ionotropic and chronotropic effects bc cAMP
  • SM - relaxation of intestine
26
Q

What are the clinical uses of glucagon?

A

SEVERE HYPOGLYCEMIA!!!! unconciouss and can’t eat sugar then use this but contraindicated in repeated hypoglycemia bc hepatic stores will be depleted

Endocrine diagnosis - give glucagon and should see insulin release or in suspected endocrine tumores bc can see increased calcitonon from medullary carcinoma or catecholamines from pheo

Beta Blocker Poisoning - increases cAMP

Radiology of bowel - relaxes it for XR visualization

LAST TEST!!! (17 decks)

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