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P34 Flashcards

1
Q

Bleomycin

A

Cytotoxic antibiotic/ anticancer agent

Actions: causes DNA fragmentation

Use: Squamous cell cancer. metastatic germ cell. Non-Hodgkin’s lymphoma

Side effects: PULMONARY FIBROSIS, skin toxicity, mucositis, transient hypersensitivity reactions. minimal myelosuppression

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2
Q

Cytarabine

A

ANTIMETABOLITE

Actions and MOA: pyrimidine analogue that is converted in the cell to triphosphate which inhibits DNA polymerase

Use: AML

Side effects: marked myelosuppression. GIT disturbance, cerebellar ataxia

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3
Q

Flurouracil

A

ANTIMETABOLITE

Actions: interferes with the synthesis of dTMP and with DNA synthesis

MOA; gives rise to a fraudulent nucleotide and inhibits thymidylate synthase

Use: Cancers of GIT, pancreas, breast, malignant skin conditions

Side effect: myelosuppression, GIT disturbance, mucositis.

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4
Q

General chemotherapy side effects

A

Gastrointestinal tract – Diarrhoea, sore mouth, nausea and vomiting

Bone marrow – Myelosuppression; can lead to anaemia, neutropenia and thrombocytopenia

Loss of hair – partial / total alopecia

Reproductivity – can affect both men and women

Tumour Lysis syndrome – Rapid breakdown of malignant cells can cause hyperuricaemia, hyperkalaemia, hypophosphataemia, hypocalcaemia with consequent renal damage / arrhythmias.

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5
Q

Carboplatin

Cisplatin

Oxaliplatin

A

CYTOTOXIC agent

Actions/MOA: forms a reactive complex that causes intrastrand CROSSLINKING and denaturation of DNA

Use: cancer of testes, ovaries, cervix, bladder, lung, head and neck

SE: Nephro/ototoxic, severe nausea and vomiting, myelosuppression, peripheral neuropathy, hypomagnesaemia

Myelosuppression is greater than cisplatin but other side effects reduced

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6
Q

Methotrexate

A

DMARD/ ANTIMETABOLITE (cancer)

Actions: marked anti-inflammatory action. Cytotoxic in large doses

MOA: Folate antagonist and therefore interferes with thymidylate synthesis (essential for DNA synthesis)

Use: RA, juvenile arthritis, psoriasis, ankylosing spondylitis, polymyositis, cancer, SLE, abortion

Side effects: GI disturbance, dose related liver toxicity, bone marrow suppression, pneumonitis

Contraindications: pregnancy, breast feeding, immunodeficiency syndromes, impaired renal or liver function

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7
Q

Vincristine

A

Vinca Alkaloid

MOA: binds to tubulin preventing spindle formation in dividing cells stopping them in mitosis

Use: leukaemia, lymphoma, breast and lung cancers

SE: nausea and vomiting, hair loss, neurotoxicity,

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8
Q

Doxorubicin

A

Class: Anthracycline, Cytotoxic antibiotic

MoA: inhibits DNA and RNA synthesis through an effect on topoisomerase II

Use: acute leukaemias, Hodgkin’s and non-Hodgkin’s lymphoma, tumours of breast, ovary, bladder, bronchi

SE: nausea and vomiting, hair loss, myelosuppression, dilated cardiomyopathy (dose dependent)

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9
Q

Cyclophophamide

A

ALKYLATING AGENT

Actions: cross links DNA by forming covalent bonds with guanine residues on each strand. interferes with cell division and triggering apoptosis.

Use: CLL, soft tissue sarcoma, osteogenic sarcoma, ovarian and breast cancer

SE: nausea and vomiting. myelosuppression, alopecia, infertility, leukaemia

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10
Q

Acute lymphoblastic leukaemia is treated with a chemotherapy combination Hyper-CVAD.

What does Hyper-CVAD involve?

A

Cyclophosphamide
Vincristine
Doxorubicin
Dexamethasone

The term ‘hyper’ refers to the hyperfractionated nature of the chemotherapy, which is given in smaller doses, more frequently, to minimize side effects.

‘CVAD’ is the acronym of the drugs used.

Course A:

  • Cyclophosphamide
  • Vincristine
  • Doxorubicin (also known by its trade name, Adriamycin)
  • Dexamethasone.

Course B:

  • Methotrexate
  • Cytarabine.

The protocol was originally developed to treat leukemia in young, fit patients, due to its intensity, but has since begun to be used more widely.

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11
Q

Acute lymphoblastic leukemia chemotherapy regime.

A

Induction – intensive treatment aimed at destroying as many leukaemia cells as possible and achieving remission (no leukaemia cells on bone marrow biopsy). Lasts 4-6 weeks.

Consolidation – aimed at remission and preventing spread. Often involves intra-spinal injections and then tablets.

Maintenance – lasts 2 years (girls) or 3 years (boys) from the start of interim treatment. Involves regular tablets and possible injections.

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12
Q

Insulin

A

Increases tissue uptake and storage of glucose, fats and amino acids. Decreases blood glucose. Inhibits glycogenolysis and gluconeogenesis. Increases glycogen synthesis; Inhibits lipolysis

MOA: binds to its receptor and causes autophosphorylation of receptor.

Use: type 1 and type 2 DM. Emergency treatment of DKA

Side effects: hypoglycaemia. weight gain.

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13
Q

Metformin

A

BIGUANIDE

Actions: Lowers blood glucose

MOA: inhibits gluconeogenesis in liver by activating AMP-activated protein kinase. Increases glucose uptake into tissues

ADE: excreted unchanged in urine. Avoid in renal insufficiency

Use: T2DM, especially if obese

Side effects: GI upset, diarrhoea, anorexia.
Rare: lactic acidosis

DOES NOT CAUSE HYPOGLYCAEMIA

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14
Q

Gliclazide

A

SULPHONYLUREA

Actions: Increased insulin release from functioning beta cells, producing insulin effects

MOA: Interaction with sulphonylurea receptor - subunit of K-ATP chanel in cell membrane of beta cells and causes K+ channels to close.
cell depolarises and activates calcium channels. Calcium channel opening stimulates exocytosis of insulin.

Use: T2DM

Side effects: hypoglycaemia. weight gain

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15
Q

Glimepiride

A

SULPHONYLUREA

Actions: Increased insulin release from functioning beta cells, producing insulin effects

MOA: Interaction with sulphonylurea receptor - subunit of K-ATP chanel in cell membrane of beta cells and causes K+ channels to close.
cell depolarises and activates calcium channels. Calcium channel opening stimulates exocytosis of insulin.

Use: T2DM

Side effects: hypoglycaemia. weight gain

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16
Q

Repaglinide

Metaglinide

A

Actions: decreased blood glucose concentration. Stimulates insulin release from beta cells

MOA: As sulphonylureas - interaction with K-ATP channel in cell membrane of beta cells and causes K+ channels to close.
Cell depolarises and activates calcium channels which stimulates exocytosis of insulin.

Use: T2DM

Side effects: hypoglycaemia

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17
Q

Pioglitazone

A

THIAZOLIDINEDIONE

Actions: decrease blood glucose concentration

MOA: activates PPAR-gamma in liver,fat and muscle to increase transcription of genes for proteins important in insulin action. Decrease glucose release from liver, increase muscle uptake and increased sensitivity to insulin.

Use: T2DM

Side effects: weight gain, fluid retention, hepatotoxic, Low risk of hypoglycaemia

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18
Q

Acarbose

A

Not used anymore.

GLUCOSIDASE INHIBITOR

Actions: delays carbohydrate absorption from intestine

MOA: Inhibits intestinal alpha-glucosidase and pancreatic amylase so decreases rise in blood glucose post-meal. It is responsible for breakdown of carbohydrates

Use: T2DM not controlled by other drugs

Side effects: GIT disturbance - flatulence, diarrhoea

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19
Q

Linagliptin

A

DPP4 inhibitor

Actions: antidiabetic. Lowers blood sugar

MOA: competitive inhibition of DIPEPTIDYL PEPTIDASE 4 that breaks down GLP-1 hormones released in response to a meal. Stopping GLP1 deactivation, increased insulin secretion and decreased glucagon

Use: T2DM

Side effects: rare. nausea, headache, hypersensitivity reaction

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20
Q

Sitagliptin

A

DPP4 inhibitor

Actions: antidiabetic. Lowers blood sugar

MOA: competitive inhibition of DIPEPTIDYL PEPTIDASE 4 that breaks down GLP-1 hormones released in response to a meal. Stopping GLP1 deactivation, increased insulin secretion and decreased glucagon

Use: T2DM

Side effects: rare. nausea, headache, hypersensitivity reaction

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21
Q

Canagliflozin

A

SGLT2 inhibitor

Action: decreased blood glucose. Decreases BP via osmotic diuresis

MOA: inhibitor of subtype 2 sodium glucose transport proteins (SGLT2) which are responsible for renal glucose absorption. Glucose is eliminated in urine

Use: T2DM

Side effects: increased UTI and genital infections. Decreased BP. Increased urination. Increased LDL and may increase risk of DKA

22
Q

Dapagliflozin

A

SGLT2 inhibitor

Action: decreased blood glucose. Decreases BP via osmotic diuresis

MOA: inhibitor of subtype 2 sodium glucose transport proteins (SGLT2) which are responsible for renal glucose absorption. Glucose is eliminated in urine

Use: T2DM

Side effects: increased UTI and genital infections. Decreased BP. Increased urination. Increased LDL and may increase risk of DKA

23
Q

Exenatide

A

GLP1 analogue

Actions: stimulates insulin secretion to decrease blood glucose

MOA: GLP1 agonist. GLP1 is released after a meal to stimulate insulin release. Slows gastric emptying. Decreased glucagon

Use: T2DM

Side effects: GIT disturbance. Dizziness or headache

24
Q

Liraglitide

A

GLP1 analogue

Actions: stimulates insulin secretion to decrease blood glucose

MOA: GLP1 agonist. GLP1 is released after a meal to stimulate insulin release. Slows gastric emptying. Decreased glucagon

Use: T2DM

Side effects: GIT disturbance. Dizziness or headache

25
Q

Empagliflozin

A

SGLT2 inhibitor

Action: decreased blood glucose. Decreases BP via osmotic diuresis

MOA: inhibitor of subtype 2 sodium glucose transport proteins (SGLT2) which are responsible for renal glucose absorption. Glucose is eliminated in urine

Use: T2DM

Side effects: increased UTI and genital infections. Decreased BP. Increased urination. Increased LDL and may increase risk of DKA

26
Q

Saxagliptin

A

DPP4 inhibitor

Actions: antidiabetic. Lowers blood sugar

MOA: competitive inhibition of DIPEPTIDYL PEPTIDASE 4 that breaks down GLP-1 hormones released in response to a meal. Stopping GLP1 deactivation, increased insulin secretion and decreased glucagon

Use: T2DM

Side effects: rare. nausea, headache, hypersensitivity reaction

27
Q

Bupropion

A

Dopamine reuptake inhibitor

Action: atypical antidepressant. elevated mood

MOA: relatively selective inhibitor of neuronal dopamine reuptake. Also antagonist at NICOTINIC receptors

Use: depression, smoking cessation

SE: Agitation, dry mouth, tremor, nausea, insomnia

28
Q

Vareniciline

A

Start 1-2 weeks before stopping

Action: decreases cravings, decrease pleasure from tobacco

MOA: nicotinic receptor partial agonist
Less effect on dopamine than nicotine

SE: mild nausea, headaches, difficulty sleeping, nightmares

Use: smoking cessation

29
Q

Nicotine replacement therapy

A

Patches, gum, nasal spray, mouth spray, inhalation, lozenge, sublingual tablet

Most effective the behavioural interventions

Contraindicated in CV disease or recent stroke

SE: Nausea, dizziness, flu like symptoms, palpitations, dyspepsia

30
Q

Spironolactone

A

Aldosterone antagonist.

MoA: Competes with aldosterone for receptor sites in the distal renal tubules, increasing sodium chloride and water excretion while conserving potassium and hydrogen ions; may block the effect of aldosterone on arteriolar smooth muscle as well.

Use: 
- Oedema in cirrhosis 
- Severe heart failure
- Conn's syndrome
(temporary treatment)
- Resistant hypertension

SE:

  • Hyperkalaemia
  • Hyperchloraemic acidosis
  • Gynaecomastia
31
Q

Eplerenone

A

Class: Aldosterone (mineralocorticoid receptor) antagonist

MoA: The potassium-sparing diuretics spironolactone and eplerenone compete with aldosterone for the mineralocorticoid receptor (MR), blocking the induction by aldosterone of the expression and activity of the epithelial Na+ channel (ENaC), the basolateral Na+/K+-ATPase pump and other aldosterone-induced proteins (AIP)

Use:

  • Oedema in cirrhosis
  • Severe heart failure
  • Conn’s syndrome (primary hyperaldosteronism in patients awaiting surgery or when surgery not option)
  • Resistant hypertension

SE:

  • Hyperchloraemic acidosis
  • Gynaecomastia, amenorrhoea
  • Hyperkalaemia
  • Vasculitis
  • Erythematous maculopapular rash
  • Steven-Johnson syndrome (T-cell mediated hypersensitivity reaction)
  • Renal insufficiency
  • Hepatotoxicity
  • Agranulocytosis
32
Q

Furosemide

Bumetanide

A

Loop diuretic

Inhibits Na/K/2Cl cotransporter in the luminal membrane of the ascending loop of henle
- Increases Na+, Cl-, water, Mg+ and Ca2+ excretion

Indication:

  • Acute pulmonary oedema
  • Chronic heart failure
  • Diuretic resistant oedema
  • Resistant hypertension (rarely used)

SE:

  • Hyponatraemia
  • Hypokalaemic acidosis
  • Hypochloraemic alkalosis
  • Hyperuricaemia
  • Hypovolaemia
  • Hypotension in elderly
  • Renal impairment (from dehydration + direct toxic effect)
  • Hyperglycaemia (less common than with thiazides)
  • Gout
  • Reversible ototoxicity (uncommon)
33
Q

Ramipril
Lisinopril
Captopril
Perindopril

A

ACEi

Indication:

  • Hypertension
  • Chronic heart failure (adjunct)
  • Prophylaxis after MI
  • Nephropathy
  • Secondary prevention in IHD / AMI / Stroke

SE:

  • Dry cough 10-20% secondary to increased bradykinin which is usually inactivated by ACE
  • Hypotension
  • Hyperkalaemia (lower aldosterone promotes K+ retention)
  • Worsen renal failure
  • Angioedema
  • Other anaphylactoid reactions

MoA:

  • Its active metabolite reversibly binds to ACE preventing angiotensin I to become angiotensin II
  • Decreased angiotensin II enhances natriuresis, lowers blood pressure, and prevents remodeling of smooth muscle and cardiac myocytes

Effects:

  • Lowered arterial and venous pressure reduces preload and afterload
  • ACE inhibitors interfere with the degradation of bradykinin (a peptide which causes vasodilation)
  • ACE inhibitors inhibit the production of angiotensin II and ARBs block angiotensin II receptors. Therefore, both classes of medication cause vasodilation of the efferent arteriole
34
Q

Define ‘pharmacodynamic drug interaction’?

How is this different to a pharmacokinetic drug interaction?

A

Pharmacodynamic drug–drug interactions occur when interacting drugs have either additive effects, in which case the overall effect is increased, or opposing effects, in which case the overall effect is decreased or even ‘cancelled out’.

Pharmacokinetic drug–drug interactions occur when one drug changes the systemic concentration of another drug, altering ‘how much’ and for ‘how long’ it is present at the site of action.

Summary:

  • Pharmacodynamic: additive or reductive drug interaction
  • Pharmacokinetic: drug interaction in which one drug alters the systemic concentration of another causing increased or decreased duration of effect.
35
Q

How do NSAIDs cause AKI?

A

NSAID-induced inhibition of PG-mediated afferent vasodilation and reduction in peritubular blood flow may also increase the risk of ischaemic acute tubular necrosis (ATN) or other nephrotoxin-induced tubular injury from drugs such as aminoglycosides, amphotericin B, hydroxyethyl starch, and radiocontrast material.

36
Q

CKD stages

A

Stage 1 with normal or high GFR (GFR > 90 mL/min)

Stage 2 Mild CKD (GFR = 60-89 mL/min)

Stage 3A Moderate CKD (GFR = 45-59 mL/min)

Stage 3B Moderate CKD (GFR = 30-44 mL/min)

Stage 4 Severe CKD (GFR = 15-29 mL/min)

Stage 5 End Stage CKD (GFR <15 mL/min)

37
Q

Canagliflozin
Empagliflozin
Dapagliflozin

A

Sodium-glucose cotransporter-2 (SGLT-2) inhibitors

MoA:

  • Prevents glucose re-uptake in renal tubules
  • Increases glucose loss in urine

Side effects:

  • Recurrent thrush
  • UTIs
  • Diabetic ketoacidosis

Constradictiatinons:
- eGFR <60

38
Q

Which diabetes drug classes cause weight gain?

A

Thiazolidinediones (glitazones)
Sulfonylureas
Meglitinides

39
Q

Which diabetes drug classes cause weight loss?

A

SGLT-2 inhibitors
GLP-1 mimetics
DPP-4 inhibitors

40
Q

Exenatide
Liraglutide
Dulaglutide

A

Glucagon-like-peptide-1 (GLP-1) mimetics

41
Q

Repaglinide

Nateglinide

A

Meglitinides (glinides)

42
Q

Gliclazide

Glimepiride

A

Sulphonylureas

43
Q

Pioglitazone

Rosiglitazone

A

Thiazolidinediones

44
Q

Metformin

A

Biguanide

45
Q

Sitagliptin

Saxagliptin

A

Dipeptidyl peptidase-4 (DPP-4) inhibitors

46
Q

Canagliflozin
Empagliflozin
Dapagliflozin

A

Sodium-glucose co-transporter-2 (SGLT-2) inhibitors

47
Q

List 4 DM II drug class suffixes.

A
  • glitazone (thiazolidinediones)
  • glinide (meglitinides)
  • gliptin (DPP-4 inhibitors)
  • gliflozin (SGLT-2 inhibitors)
48
Q
  • glitazone
  • glinide
  • gliptin
  • gliflozin
A

(-glitazone):

  • Thiazolidinediones
  • Pioglitazone, lobeglitazone, rosiglitazone

(-glinide):

  • Meglitinides
  • Repaglinide, nateglinide

(-gliptin):

  • DPP-4 inhibitors
  • Sitagliptin, saxagliptin

(-gliflozin):

  • SGLT-2 inhibitors
  • Canagliflozin, empagliflozin. dapagliflozin

The others don’t have a notable prefix/suffix

Biguanide:
- Metformin

Sulfonylureas:

  • Gliclazide
  • Glimepiride

GLP-1 mimetics:

  • Exanatide
  • Liraglutide
49
Q

List all DMII drug classes

A
  • Biguanides
  • Thiazolidinediones (glitazones)
  • Sulfonylureas
  • Meglitinides (glinides)
  • Dipeptidyl peptidase-4 (DPP-4) inhibitors
  • Glucagon like peptide-1 (GLP-1) mimetics
  • Sodium-glucose cotransporter-2 (SGLT-2) inhibitors
50
Q

List all secretagogues and sensitisers (DM II drugs).

List other drug classes that don’t fit into either category.

A

Sensitisers:

  • Biguanides
  • Thiazolidinediones (glitazones)

Secretagogues:

  • Sulfonylureas
  • Meglitinides (glinides)
  • Dipeptidyl peptidase-4 (DPP-4) inhibitors
  • Glucagon like peptide-1 (GLP-1) mimetics

Other (renal excretor):
- Sodium-glucose cotransporter-2 (SGLT-2) inhibitors

51
Q

AKI staging

A

Stage 1: creatinine 1.5-2x normal, urine output <0.5mL/kg/hr for 6 hours

Stage 2: 2-3x normal, urine output <0.5mL/kg/hr for 12 hours

Stage 3: >3x or RRT, urine output <0.3mL/kg/hr for 24 hours or anuria for 12 hours

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