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GSS > GSS Past Paper Qs > Flashcards

GSS Past Paper Qs Flashcards

1
Q

Excess acid in the stomach can cause

A

Heart Burn

Indigestion

Acid Reflux

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2
Q

name key sells found in the gastric glands

A
  1. Chief Cells
  2. Parietal Cells
  3. Mucus secreting cells
  4. Hormone secreting Cells
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3
Q

what does stomach acid do?

A

deactivates ingested bacteria and denatures ingested proteins to allow for efficient protease reactions

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4
Q

Here is a picture of histamine conformers. Which of the two conformations bind to H1 and H2?

A

The trans conformer. It has les steric hinderance than gauche

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5
Q

What is the name of this molecule and what is its pka, and shape in space

A

Guanidine - pKa = 14.5, planar shape

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6
Q

Here are some groups. What is their pKa values? Additionally, what is the pKa value of aliphatic amines, and what is the pka of an aromatic amine?

H

Ph

Ch3CO

NH2CO

MeO

CN

NO2

A

aromatic amines have pH of 4

Aliphatic amine has a pKa of 10

H = 14.5

Ph = 10.8

Ch3CO = 8.33

NH2CO = 7.9

MeO = 7.5

CN = -0.4

NO2= -0.9

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7
Q

What groups are critical for H2 receptor antagonist activity

A

Sulfur introduced an inductive effect on the side chain and also the CH3 introduced an inductive effect at C5, resulting in increase in electron densitiy at N1 and a decrease in electron density at N3. This facillitates the dissociation of the N3-Hydrogen to predominate the desired tautomer that characterises antagonist activity.

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8
Q

What is this structure and what is the pKa of the ring? and What makes it a successful drug?

A

Cimetidine - it has an imidazole ring which has a pKa of 14.5. if present the ‘t’ tautomer will predominate and it will be selective to H2 receptors.

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9
Q

what is this structure suggest why it lasts longer than cimitedine

A

Ranitidine - The tertiary amine side chain allows the formation of salts

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10
Q

what is this structure and how does it work, what is it’s pKa and why is it so goddamn specific

A

Omeprazole - Proton Pump Inhibitor. It is a prodrug that is tranformed within the acidic canaliculi of the parietal cells to its active form, a sulfenamide.

The sulfenamide reacs with thiol groups in the ATPase enzyme, forming a disulfide link which inactivates the enzyme.

it has a pKa of 4.0 and is a weak base. Thus it is ionised in the stomach into its active species. Specific because This active species is a permanent cation and cannot escape the canaliculi.

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11
Q

Provide the mechanism for Omeprazole that forms this the active sulfenamide

A
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12
Q

what determines the extent to which the PPI accumulates in the canalicular lumen?

A

the pKa and the hydrophobicity

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13
Q

How do glucose meters work?

A
  1. The meter is first calibrated to match the test strip
  2. When blood is placed onto the test strip, it reacts with a glucose oxidase producing gluconic acid from the glucose in the blood.
  3. At the other end of the test strip, the meter tranfers a current to the test strip.
  4. The Test strip has electric terminals which allow the meter to measure the current between the terminals
  5. At the electrode surface, the current is detected. Measures the amount transferred.
  6. can take up to 5-60 seconds depending on model
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14
Q

state the key liver enzymes and how they function

A

Alanine aminotransferase (ALT)

Aspartarte aminotransferase (AST)

Alkaline phosphatase (ALP)

Gamma glutamyl transferase (GGT or ‘Gamma GT’)

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15
Q

how does the liver influence drug metabolism

A
  • Distribution of drugs may be altered:
  • ↓ protein binding in cholestasis as bile is diverted from hepatocytes to blood + competes for protein binding sites
  • Ascites - drugs may deposit in peritoneal cavity
  • Elimination may be reduced in cholestasis reduced formation of water-soluble conjugates that can be excreted.
  • For high extraction ratio drugs (i.e drugs that face high first-pass metabolism) they may experience increased bioavailablility
  • varices formation may mean drugs can bypass liver alltogether.
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16
Q

Senna Calculates the percentage content of hydroxyantracene glycosides expressed as sennoside B. Rather than sennoside B itself. Why?

A

It is very difficult to separate the individual sennosides in Senna (A,B,C,D)

In order to calculate the extinction coefficient, the molecular weight of each sennoside is required

All the sennosides have the same biological activity

Sennosides: A + B = same molecular weight

Sennosides C + D = give same UV absorption as A and B

17
Q

state how the skin is involved in temperature regulation

A
  • Blood vessel innervation to dermis
  • Heat exchange regulates body temperature via regulation of heat gain and heat loss
  • Heat loss is regulated by altering blood flow through the capillaries in the dermal papillae
  • Vasodilation stimulated by local production of bradykinin
  • arrector pili muscle contracts and relaxes.
18
Q

state antiemetic drugs and their mechanisms

A

5HT3 Antagonists: Ondansetron (post-op nausea and vomiting)

D2 Antagonists: Domperidone, Prochloperazine

Inhibitors of the Vomiting Centre: Hyoscine, Promethazine

Dexamthazone: Anti-emetic corticosteroid (post-op nausea and vomiting)

19
Q

5 conditions for topical steroids

A
  1. Insect Bite and Sting Reactions
  2. Atopc Eczema
  3. Atopic Dermatitis
  4. Psoriasis
  5. Inflammation of the external ear (Otitis Externa)
20
Q

cold sores. what is it and otc treatment

A

caused by herpes simplex virus - treated with aciclovir antiviral agent.

can also give Anaesthetics for symptomatic relief e.g lidocaine

21
Q

what is psoriasis and how to treat

A
  • Chronic inflammatory skin disease
  • Increased epidermal cell turnover thickening and scaling
  • Inflammatory cell infiltration
  • Relapsing

Can be caused by:

  1. Stress
  2. Drugs (b-blockers, lithium, antimalarials, withdrawal of systemic steroids)
  3. Streptococcal infection
  4. Hormonal events
22
Q

what is eczema and how does it differ from dermatitis

A

Impaired barrier function

  • Maybe due to defect in lipid production that normally holds keratinocytes firmly together
  • Causes great water loss, dry cracked skin
  • Easier entry of irritants and allergens cause an inflammatory

response

• Acute Vs Chronic

23
Q

mechanisms of drugs to increase their absorption into skin

A

Penetration enhancers (e.g Urea)

Pro-drugs to enhance lipophilicity

Ion pairing - pairing up the drug with an ion e.g lidocaine hcl to cross stratum corneum

Changing the thermodynamic activity of drug (super saturated systems),

vesicles (liposomes)

24
Q

what are the phases of acid secretion

A
25
Q

ten key points about skin physiology

A
  1. Largely there as a protective barrier against external forces; protects against loss of moisture, microbial infection etc.
  2. Stabilises blood pressure and temperature (site of heat loss for the body)
  3. Mediates sensitisation of Temperature, touch and pain
  4. HYPODERMIS (subcutaneous tissue - fatty insulating layer; at the very base of the skin)
  5. DERMIS (The middle layer of the skin of which contains blood vessels, hair follicle and sweat glands)
  6. EPIDERMIS (The top layer of the skin)

The epidermis provides one of the major barriers to drug absorption through the skin.

  1. Stratum corneum is the site for suncreens, antimicrobials and antiseptics
  2. Lower epidermis is the site for corticosteroids, cytotoxics and antiviral and antihistamines.
  3. appendages - sites of antimicrobials, acne and infection of follicle treatment
  4. deeper tissues/systemic - site of hormones and nicotine
26
Q

what is the importance of bile salts and what mechanisms are fats absrobed across the small intestine

A
27
Q

alcohol withdrawal signs and treatment

A
28
Q

Potts and Guys Equation

A
29
Q

RTS Acne. What drugs could make it worse?

A

high progestogen oral contraceptives, lithium

Treatments:

Salicylic acid & salicylates

Mode of action: antifungal property of salicylic acid helps promote shedding of cells from skin surface. It is effective against non-inflammatory acne lesions as it unclogs pores

Benzoyl peroxide

  • Mode of action: antibacterial & removes dead skin cells
  • Over 12 Years old
  • Start on lower strengths
  • ok in pregnancy

Light therapy

Oxy Clearlight

light therapy at a specific and safe wavelength to trigger a biological reaction that kills the P.acnes bacteria which in turn leads to reduced inflammation and healing

Self care

  • Do not wash more than twice a day.
  • Use a mild soap / cleanser + lukewarm water
  • Do not scrub / use abrasive soaps, cleansing granules, astringents, or exfoliating agents (advise use of a soft
  • wash-cloth and fingers instead).
  • Should not attempt to ‘clean’ blackheads. Scrubbing or picking acne is liable to worsen the condition.
  • Ideally, should avoid excessive use of make-up and cosmetics (non-comedogenic, water-based product
  • should be used sparingly)
  • Remove makeup at night.
  • Use a fragrance-free, water-based emollient if dry skin is a problem (several topical acne drugs dry the
  • skin). The use of ointments or oil-rich creams should be avoided as these can clog pores.
30
Q

5 local side effects and 2 systemic side effects of topical corticosteroids

A
  1. Spread and worsening of untreated infection
  2. thinning of the skin
  3. Reddening of skin
  4. stretch marks
  5. contact dermatitis

Systemic:

Adrenal suppression; cushings syndrome

31
Q

5 examples of steroids and doses

A

Hydrocortisone cream 1% - mild inflammatory skin disorders e.g eczemas and nappy rash 1-2bd

Clobetasone Butyrate 0.05% - more potent, for Eczema and dermatitis of all types. 1-2bd

Bethamethasone Valerate 0.025% - severe inflammatory disorders such as eczemas that were unresponsive. 1-2bd

Clobetasol Propionate 0.05% - Psoriasis 1-2bd for 4weeks max 50g per week

32
Q

classes of steroids and their uses

A

Adrenal Corticoids e.g Prednisolone

Estrogens e.g transdermal delivery of estradiol

Androgens - Testosterone gel to increase testosterone

Progesterones

Anabolic steroids

33
Q

Outline the two proposed mechanisms of corticosteroids

A

Genomic action and Non Gemonic action (faster)

Genomic:

Specific binding to cytoplasmic nuclear receptors occurs. Other transcription factors may be involved.

Gene activation or repression occurs by direct DNA binding of the steroid-receptor complex to recognition sites in the promoter regions associated with up-regulation or down-regulation.

Gene repression can occur through protein-protein cross talk.

Non-Genomic:

Involves Membrane bound steroid receptors, Intracellular receptors and other non-specific actions. Glucocorticoids at @ gene level to reduce inflammation by promoting transcription of some genes and inhibiting transcription of others.

34
Q
A
35
Q

what are the 5 key LFTs

A

Test Parameters:

Albumin

Hypoalbuminaemia = feature of advanced chronic liver disease (LD)

Bilirubin

An increase means a blockage in bile flow

Aminotransferase (AST and ALT)

An increase means hepatocellular damage

Gamma-glutamyltransferase (γGT)

Sensitive to drugs and alcohol

Alkaline phosphatase (ALP)

An increase means blockage of bile flow

GSS (10 decks)

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