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Pharma > Thuroid & Diabetes > Flashcards

Thuroid & Diabetes Flashcards

0
Q

MOA thioureylens

Carbimbazine & PTU

A

Blocks enzyme which synthesise thyroid hormones

PTU also prevent T4-T3 conversion in peripheral tissue

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1
Q

First line agents against hyperthyroidism

A

Thioureylenes
Carbimazole
Propylthiouracil PTU

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2
Q

What is the drug of choice in hypothyroidism?

A

Thyroxine T4 (synthetic)

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3
Q

Insulin

A

2 amino acid chains produced & stored in Beta cell in islet of langerhans in the pancreas

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4
Q

Hyperglycaemia

A

Elevated glucose levels

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5
Q

HbA1c

A

Glycated haemoglobin

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6
Q

Diabetes is

A

A metabolic disorder characterised by chronic hyperglycaemia with disturbance of carbohydrate, fat & protein metabolism resulting from defects in insulin secretion, lack of insulin sensitivity or both

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7
Q

Normal BGL

A

3.5-8mmol/L

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8
Q

Action of insulin

A
  • Increase glucose and amino acid uptake by muscle, liver and adipose tissue
  • increases protein synthesis, glycogenesis, loop genesis RNA &DNA synthesis intracellular action(growth)
  • reduces glucose output, glyconeogenesis, proteolysis & lipolysis
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9
Q

First line oral hypoglycaemic agents in type 2 diabetes treatment

A

Metformin

Biguanides

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10
Q

Second line oral hypoglycaemic agent in the treatment of diabetes 2

A

Sulfonylureas

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11
Q

Sulfonylureas action

A

Closes K+ ATP channel stimulates release of insulin from beta cells in pancreas

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12
Q

HbA1C

A

Below 7% significantly reduces risk of complications

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13
Q

Haemersiderin deposits

A

Painful, itchy, dry brown iron deposits

Anterior tibia

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14
Q

How do we treat a bacterial infection where MRSA is present?

A

Vancomycin

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15
Q

When must you give people diabetes education?

A

Every time they come into clinic

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16
Q

Pharmacological anxiety treatments

A

Benzodiazepines
Antidepressants
Antipsychotics

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17
Q

Role of GABA

A

Inhibitory neurotransmitter in the CNS

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18
Q

MOA benzodiazepines

A

Bind to GABAa receptor –> greater response to GABA –> reduced anxiety

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19
Q

SSRI

A

Selective serotonin re-uptake inhibitors

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20
Q

SNRIs

A

Serotonin & noradrenalin re-uptake inhibitors

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21
Q

TCAs

A

Tricyclic antidepressants

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22
Q

MOA-Is

A

Monoamine oxidase inhibitors

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23
Q

Non pharmacological treatments of depression

A 
Monitor
Educate
Supportive counselling
Guided self-help
Behavioural techniques
Psychotherapy
Physical exercise & lifestyle change
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24
Q

SSRIs MOA

A

Selective serotonin re uptake inhibitor: Selectively inhibits presynaptic re-uptake of serotonin into nerve terminal

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25
Q

SNRIs MOA

A

Serotonin & noradrenalin re-uptake inhibitors: inhibit serotonin and noradrenalin re uptake

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26
Q

TCAs MOA

A

Tricyclic antidepressants: inhibit noradrenaline & serotonin uptake (to presynaptic terminals)

Also blockcholinergic, histaminic, alpha receptors –> ADRs

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27
Q

MAO-I MOA

A

Monoamine oxidase inhibitors

Irreversibly inhibit an enzyme MAO-A and MAO-B increasing concentration of all amines

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28
Q

Simvastatin MOA

A

HMG-CoA reductase inhibitor

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29
Q

Alpha glucose inhibitor example and MOA

A

(Acarbose) inhibits the enzyme in the small intestine and delays digestion & absorption of polysaccharide carbohydrates

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30
Q

Glitazones examples and MOA

A

(Thiazoledinediones)
Pioglitazone
Rosiglitazone
Increases sensitivity in peripheral tissues to insulin, regulates glucose and lipid metabolism, decreases glyconeogenesis (liver glucose output)

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31
Q

Gliptins

DPP4 inhibitors

A

Inhibit DDP enzyme - increase in retain levels & beta cells glucose sensitivity
–> increase glucose dependant insulin secretion –> decrease glucagon & so decrease glucose production –> increase insulin synthesis

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32
Q

Incretin analogues

Example and MOA

A

Exenatide, litaglutide

  • increase glucose dependant insulin secretion
  • decrease inappropriate glucagon secretion
  • delays gastric emptying, rate of glucose absorption and reduces appetite
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33
Q

Biguanides

Example & MOA

A

Metformin

  • decrease glucose production
  • increase glucose uptake by AMP-K activity in cell membrane
  • reduce glucose absorption
  • increase fatty acid oxidation
  • increase sensitivity & binding
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34
Q

First line treatment for diabetes

A

Biguanides

Metformin

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35
Q

Sulfonylureas

Example and MOA

A

Glibenclamide, clipzide, gliclazide, glimepiride

Closes K+ATP channel stimulates release of insulin from beta cells in pancreas

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36
Q

Sulfonylureas

Can

A

Reduce insulin resistance
Or
Increase insulin sensitivity

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37
Q

Cramping is due to

A

Ischaemia

Intermittent claudication

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38
Q

Clotting factors

A

Proteolysis proteins made in the liver

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39
Q

Warfarin

A

Is an anticoagulant/anti thrombotic.
Works by inhibiting the synthesis of vitamin k dependant coagulation factors

(Coumadin, Marevan)

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40
Q

Miconazole

A

Daktarin

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41
Q

Lamisil
Active ingredient
Class
MOA

A

Terbinafine is an allylamine
Broad spectrum antifungal
Blocks the biosynthesis of ergosterol resulting in an accumulation of squalene

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42
Q

What is leukonychia

A

White marking on the nail
Striata
Punctata
Totalis

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43
Q

Step 1 on the pain ladder

A

Non-opioid

+/- adjuvant

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44
Q

Step 2 on the pain ladder

A

Opioid +/- non-opioid +/- adjuvant

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45
Q

Step 3 on the pain ladder

A

Opioid +/- non opioid +/- adjuvant

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46
Q

Ester and amide LA clinically relevant differences

A

Esters are metabolised more quickly

Therefore shorter duration of action

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47
Q

3 characteristics of COPD treatment

A

Improve exercise tolerance
Symptom relief
Maintain or improve
Prevent or treat exacerbation a and complications

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48
Q

3 adjuvants used for pain management

A 
GABA analogues
Capsaicin
Tricyclics antidepressants
Corticosteroids
Psychotropic drugs
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49
Q

What are symptom controllers for treatment of asthma?

A

LABA

50
Q

Clinical types of pain

A

Nociceptive pain
Neuropathic pain
Mixed pain

51
Q

What micro organisms are associated with ecthyma

A

Streptococcus & pseudomonas

52
Q

Different types of DMARDS

A 
Gold salts
Penicillamine
Sulfasalazine
Hydrochloroquine
TNF-alpha antagonists 
Immunosuppressants
Cytokine modulators
53
Q

Examples of gold salts

A

Auranofin & aurothiomalate

54
Q

Penicillamine

Action

A

Reduces T-cells activity & reduces rheumatoid factor & immune complexes in blood & joints

55
Q

Sulfasalazine

MOA

A

Modifies lymphocyte proliferation

& reduces cytokines

56
Q

First line treatment in early rheumatoid arthritis

A

Methotrexate

Antimetabolite antineoplastic agent

57
Q

Onycholysis possible aetiologies

A 
Idiopathic
Systemic (PAD, iron deficiency anaemia)
Cutaneous disease(psoriasis, eczema, hyperhidrolosis)
Local causes (trauma, infection, exposure to irritants)
58
Q

In case of a penicillin allergy what is commonly used

A

Cephalosporins

59
Q

Allopurinol MOA

A

Reduces uric acid production by inhibiting a converting enzyme which converts purines to uric acid
(Reduces plasma and urinary irate levels)

60
Q

Name 3topical antifungal nail lacquer

A

Amorolfine- loceryl
Bifonazole- canestan nail treatment
Ciclopirox- rejuvenail

61
Q

What is used to treat Methicillin resistant staphycoccus aureus?

A

MRSA

Vancomycin- inhibits bacterial cell wall synthesis (glucopeptide)

62
Q

Prednisone

A

Corticosteroid

63
Q

Corticosteroid MOA

A

Regulate gene expression suppressing inflammation & immune response as well as glucose, protein & lipid metabolism.

Mimic action of body’s own steroids.

64
Q

Uniform thickening of the nail

A

Onychauxis

65
Q

Three types of involuted nails

A

Tile shaped
Plicatured
Pincer

66
Q

Onychogryphosis

A

Nail plate grossly thickened & curved

May have longitudinal or transverse ridges

67
Q

Onychomycosis

A

Fungal infection of nail bed and nail plate
Involves dermatophytes metabolising keratin
Causes nail plate to thicken and discolour

68
Q

Onycholysis

A

Separation of the nail from the nail bed at distal end &/or lateral margins
Detachment of nail plate leads to greyish-white colour

69
Q

Spontaneous separation of the nail

From matrix to free edge

A

Onychomadesis

70
Q

Nail penetrates dermis in sulci

A

Onychocyptosis

71
Q

Tranexamic acid

MOA

A

Blocks binding plasminogen & plasminogen to fibrin

- inhibits breakdown of clots

72
Q

Vitamin K antagonists

MOA examples

A

Inhibit enzymatic synthesis of vitamin K dependent clotting factors & the anti thrombin factors proteins C & S

Warfarin (coumadin, marevan)
Phenindione (dindevan)

73
Q

Anticoagulants

A

Heparin
Enoxaparin
Dalteparin
Danaparoid

74
Q

MOA of heparin

A

Inactivate thrombin IIa and clotting factor XA by binding to antithrombin III

75
Q

Antiplatelet agents

A 
Aspirin 
Dipyridamole
Ticagrelor
Thienopyridines
Glycoprotein IIb/IIIa inhibitor
76
Q

Aspirin MOA

A

Irreversibly inhibit cyclo-oxygenase –> inhibit thromboxane A2 production –> blocks platelet aggregation for life of platelet

77
Q

Thrombolytics

MOA

A

Converts plasminogen to plasminogen which catalyses breakdown of fibrin

78
Q

Internal normalised ratio

A

Time taken for blood to clot using a standardised test.

79
Q

High INR is indicative of

A

The longer it will take blood to clot

Risk of bleeding

80
Q

Lower the INR

A

More likely to form a blood clot

81
Q

INR normal value

A

0.8-1.2

82
Q

Prothrombin time

A

PT - is also a measure of how long it takes blood to clot

83
Q

Target INR for people taking warfarin

A

2-3

84
Q

Onychophosis

A

HK or heloma durum in the nail sulcus

85
Q

Lipitor

Class & MOA

A

Hypolipidaemic agent - atorvastatin

MOA - HMG-CoA reductase inhibitor

86
Q

First line treatment for acute gout

A

Indomethacin (NSAID)
Or
Colchicine (if NSAID is contraindicated)

87
Q

Recurrent gout treatment

A

Allopurinol plus either colchicine or NSAID then allopurinol alone

88
Q

Chronic gout treatment

A

Difficult to treat

Colchicine and/or indomethacin are introduced slowly

89
Q

First line treatment of rheumatoid arthritis

A

Methotrexate as mono therapy OR in combination with DMARDs

90
Q

Allopurinol

MOA

A

Inhibits xanthine oxidase which catalyses the conversion of hypoxanthine to xanthine & then xanthine to urate/uric acid

91
Q

Pale dendritic cells responsible for immunological responses of skin to environmental antigens

A

Langerhans cells

92
Q

Melanocytes

A

Produce pigment & UV protection

93
Q

Merkel cells

A

Associated with nerve fibre - play a sensory function

94
Q

Specialised skin Cell with branching process

A

Melanocytes

95
Q

Pacinian corpuscule

A

Detect pressure & high frequency vibrations; largest of encapsulated nerve endings

96
Q

Ruffini endings detect

A

Heavy and continuous touch sensations & pressure

97
Q

Meissner’s corpuscle

A

Detect touch and low frequency vibration

98
Q

Merkel’s disc

A

Is primarily involved in touch

99
Q

Nerve supply of the skin

A

Autonomic nerves supply the blood vessels, sweat glands and arrector pili muscles

100
Q

Apocrine sweat glands

A

Larger than eccrine glands

Most numerous around axillae, perineum, areolae

101
Q

Eccrine sweat gland

A

Excretory duct spirals upward to open onto skin surface

Most on palms, soles, axillae & forehead

102
Q

Sweat glands

A

Tube like, cooled glands, located within the dermis
Produce a watery secretion
Two types: eccrine & apocrine

103
Q

Sebaceous gland

A

Form around hair follicle and secrete sebum

104
Q

What is the process of the entire cell being shed as a secretory product

A

Holocene process

105
Q

Papillary dermis

A

Closer to the surface- highly vascular & has a thin network of collagen fibres

106
Q

How does penicillin work?

A

Inhibit cell wall synthesis

107
Q

How does an ACE inhibitor lower BP

A

Blocks conversion of angiotensin I to angiotensin II which results in reduce vasoconstriction & reduced BP. Also reduces aldosterone release lowering sodium and water resorption reducing BP

108
Q

What causes gout?

A

Hyperuricaemia either

Decreased excretion of uric acid or increased production of uric acid

109
Q

What would you use to treat Candida albicans and trichopyton rubrum?

A

Lamisil (terbinafine) or daktarin (azole)

As they are active against both organisms

110
Q

Terbinafine & azole a work by

A

Inhibit cell wall synthesis by inhibiting ergosterol synthesis

111
Q

Yellow pus on a bacterial infection is indicative of

A

S. Aureus

112
Q

Mupirocin

A

Inhibits bacterial protein synthesis

By reversible and specifically binding to transfer RNA synthase

113
Q

First line treatment for dyslipidemia

A

Diet

114
Q

The name given to an infection that occurs during antimicrobial treatment

A

Superinfection

115
Q

Causative organisms for tinea pedis

A

Candida albicans & trichopyton rubrum

116
Q

Green fruity Purulent exudate, what micro organism would you suspect?

A

Pseudomonas

117
Q

What is treatment of choice for mild impetigo on the leg?

A

Mupirocin (Bactroban)

118
Q

4 mechanisms of antibiotics

A

Inhibit bacterial cell wall synthesis
Inhibit protein synthesis
Inhibit DNA synthesis
Disrupt or alter cell membrane permeability

119
Q

Erythromycin

MOA

A

Macro life antibiotic

Inhibits protein synthesis

120
Q

First line pharmacological treatment for congestive heart failure

A

Ace inhibitor

121
Q

Glucosamine

A

Natural supplement derived from shellfish

Thought to inhibit pro-inflammatory mediators in the development of OA

122
Q

What do you tell a patient who is using Tea tree oils instead of medicament

A

Has not been demonstrated to be consistently effective

123
Q

Paracetamol

MOA

A

Inhibit prostaglandin synthesis in CBS by inhibiting cox-3

Pharma (6 decks)

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