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revision Flashcards

1
Q

ag3

antifungal: amphotericin B & nystatin

A

MOA: binds to ergosterol in fungal cell membrane, form pores, increase permeability to proteins, causing cell death

AE: nephrotoxicity (esp when combined with aminoglycosides and cyclosporine), chills & fever

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2
Q

ag3

antifungal: ketoconazole, fluconazole, itraconazole

A

MOA: inhibits 14-alpha-demethylase, interrupt synthesis of ergosterol, accumulation of toxic intermediate sterols and inhibit fungal growth

AE: gynaecomastia

*itraconazole used to prevent Invasive aspergillus

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3
Q

ag3

antifungal: terbinafine

A

MOA: inhibit squalene epoxidase, inhibit synthesis of ergosterol

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4
Q

ag3

antifungal: caspofungin (echinocandin)

A

MOA: inhibit 1,3-beta glucan synthase, depletion of beta-glucan polymers, block cell wall synthesis

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5
Q

ag3

antifungal:
flucytosine
griseofulvin

A

flucytosine (also anticancer)
MOA: converted to 5-fluorouracil, 5-FU phosphorylated, inhibits RNA & DNA.

AE: N/V/D, bone marrow suppression

griseofulvin
MOA: inhibit mitotic spindle formation, inhibit fungal cell mitosis
Uses: Ringworm/dermatophyte infection

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6
Q

ag3

oxytoxic: oxytocin

A

MOA: bind to G protein coupled oxytoxic receptors on uterine smooth muscle cells, release IP3, increase intracellular Ca, uterine contractions
Uses: INDUCTION OF LABOUR

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7
Q

ag3

oxytoxic:ergometrine

A

MOA: cause body, fundus, cervix to contract (low dose=relaxation btwn contraction; high dose=continuous contraction)
Uses: POST PARTUM HAEMORRHAGE, 3RD STAGE LABOUR
CI: during INDUCTION OF LABOUR

*use oxytocin over ergometrine because:
-shorter half life, slow IV infusion, easy control intensity
-lower segment of uterus not contracted, foetal descend not compromised
-uterine contractions consistently augmented
-normal relaxation btwn concentrations if low conc.

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8
Q

ag3

oxytoxic:
mifeprostone
misoprostol (PGE1)
dinoprostone (PGE2)
carboprost (PGF 2 alpha)

A

-mifeprostone: terminate pregnancy
-misoprostol, dinoprostone, carboprost promote cervical ripening/cervical softening + thining and dilation of cervix= facilitate labour

*carboprost for postpartum hemorrhage

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9
Q

ag3

tocolytic:
nifedipine (CCB)-tachycardia, HoTN
atosiban (oxytocin R antagonist)
ritodrine (beta 2 agonist)-tremors
salbutamol (beta 2 agonist)-tremors

A

promote relaxation of uterus

*stages of labour
stage 1: cervix relaxes, dilates, thins out. Contractions began
stage 2: contractions increase in freq & force until infant is delivered
stage 3: uterus must contract to expel placenta

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10
Q

ag3

OCP:
-oestrogen+progesterone (monophasic, diphasic, triphasic)
-minipills/progesterone only

A

MOA: constant level of oestrogen and progesterone=insufficient thickening of endometrium=prevent implantation, decrease FSH & LH via negative feedback to hypothalamus.

*prevent ovary and endometrial CA
*interact with rifampicin and phenytoin, decrease effectiveness of OCP

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11
Q

ag3

post coital pill: levonorgestrel (emergency)
injectable progestin: medroxyprogesterone acetate

A

-levonorgestrel: release progesterone, cervical mucus & endometrium effect
-medroxyprogesterone acetate: supress ovulation and thicken cervical mucus in high levels of progestin

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12
Q

ag3

selective oestrogen receptor modulators:
clomiphene (antagonist at hypothalamus=increase GnRH)
tamoxifen (antagonist at breast)
raloxifene (agonist at bone)

A

clomiphene: treat infertility
tamoxifen: breast cancer
raloxifene: tx osteoporosis

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13
Q

ag3

nocturnal pulsatile secretion of GnRH brings on puberty

in girls which develop first? in boys?

A

girls: thelarche (breasts), pubarche (axillary and pubic hair caused by DHEA secreted by zona reticularis of adrenal cortex) then menarche (first period)

boys: testes; penis, scrotum & hair according to tanner staging; axillary hair, wet dream, peak growth….

*read up on: hypogonadotropic hypoganadism, hypergonadotropic hypogonadism, defects in HPA axis like Kallmann syndrome

*postmenopause: increased LH & FSH, decreased estrogen

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14
Q

ag2

anti-herpes

A

herpes virus: HSV-1, HSV-2, VZV, CMV

1.acyclovir for HSV1, HSV2 and VZV. If resistant, then use foscarnet
2.ganciclovir for CMV. If resistant, then use foscarnet (inhibit viral DNA and RNA polymerase)

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15
Q

ag2

anti-hepatitis

A

HBV: interferon alpha, tenofovir, lamivudine

HCV: ribavirin, ledipascir, sofosbuvir

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16
Q

ag1

pancreatic carcinoma

*endocrine cells (islet of Langerhands) mostly at tail 20%
exocrine 80%

A

genes: KRAS activation, p-16 inactivation

Due to smoking, alcholism, fat rich diet
carcinoma at head of pancreas

morphology:
-malignant glands atypical, small, irregular, bizarre
-poorly differentiated adenocarcinoma
-glandular structures with abnormal nuclei
-lymphatic invasion and dense stromal fibrosis/scarring

clinical features:
-migratory thrombophlebitis (Trousseau):clot in vein appear and disappear
-tumour markers: CEA, CA19-9 increase

Mx:
Whipple operation

17
Q

ag1

types of colitis
1. Ulcerative colitis and Crohn’s disease
2. pseudomembranous colitis
3. infective (Amoebic, TB)
4. Ischaemic & radiation

A

pseudomembranous colitis due to infection by Clostridium difficle. Occurs after use of clindamycin, sensitive to vancomycin. On sigmoidoscope: scattered yellow white membrane plaques of fibrin, leucocytes

infective colitis
-by amoebic colitis: infxn by E. histolytic
T.B colitis
-by ingested bovine bacilli

*caseating granuloma: necrosis in center
non caseating granuloma (like onion, whorl-like)

18
Q

ag1

drugs for peptic ulcers

A
  1. proton pump inhibitior (1st line)
    -omeprazole: irreversible inhibition of proton pump H+/K+ ATPase, inhibit basal and stimulated acid secretion. Used in Zollinger Ellison syndrome. Avoid long term coz pseudomembranous colitis
  2. H2 receptor inhibitor
    reversibly block H2 receptors on parietal cells, inhibit histamine induced gastric secretion. Promote mucosal healing and decrease pain
    -cimetidine: AE is gynecomastia, impotence, galactorrhea
    -ranitidine
  3. Anticholinergics
    -pirenzepine: block muscarinic M1 receptor on parietal cells, inhibit gastric acid secretion
  4. Antacids
    bind to HCL, increase pH, neutralises acid, inhibit pepsin
    -sodium bicarb (stomach distension due to CO2), calium carbonate, [aluminium OH causes constipation and Mg OH causes diarrhea= used together to avoid AE]
  5. Mucosal protective agents
    -sucralfate: coat ulcers
    -misoprostol:increase mucus and bicarb and BF, promote ulcer healing [prevent NSAID induced peptic ulcer] DO NOT GIVE IN PREGNANCY, CAUSE ABORTION
    -bismuth: coat ulcer, decrease pepsin, increase mucus & bicarb, bactericidal effect [treat traveller’s diarrhea]
19
Q

ag1

triple and quadriple therapy for H. pylori

A

triple therapy: OCLAM
omeprazole-increase stomach pH, antimicrobial
clarithromycin
amoxicillin/change to metro if allergic

quadraple therapy: OBMT
omeprazole
bismuth
metronidazole
tetracycline

20
Q

ag1

drugs for IBD (crohns and UC)

A
  1. anti-inflammatory drugs
    -sulfasalazine: 5-aminosalicylic acid anti-inflammatory and sulfapyridine antibacterial. Inhibit production of IL-1 and TNF-alpha.
    -prednisolone (glucocorticoid): produce protein that inhibit phospholipase A2
  2. immunosupressive drugs
    -azathioprine/6-mercaptopurine: impair purine biosynthesis & cell proliferation
    -methotrexate: binds to dihydrofolate reductase, no conversion of folic acid to DHF and THF, no DNA synthesis
    -cyclosporine
    3.biological agent
    -infliximab: neutralise TNF alpha
21
Q

ag1

drugs for GI infestations

A

1.cephalosporin (beta lactam antibiotic)
cell wal synthesis inhibitor: covalently bind to active site of penicillin binding protein, inhibit transpeptidase reaction, alter peptidoglycan synthesis, cell dies, bactericidal

1st-cephalexin
2nd-cefuroxime
3rd-ceftriaxone can cross BBB
4th-cefepime
5th-ceftaroline

2.quinolones
-ciprofloxacin: prevent relaxation of supercoiled DNA, inhibit topoisomerase IV

22
Q

nl1

back muscles

A
  1. splenius
    -splenius capitis
    -splenius cervicis
  2. erector spinae (ILS)
    -iliocostalis m.
    -longissimus m.
    -spinalis
  3. transversospinalis m.
    -semispinalis
    -rotators
    -multifidus
  4. suboccipital (got suboccipital triangle which vertebral artery passes through
    -4 muscles
23
Q

nl1

corticosteroid drugs MOA: inhibit inflammatory mediators, activate anti-inflammatory mediators, inhibit genes that code for cytokines like IL-2, reduce T cell proliferation & activity in. macrophages, suppress B cell func

A

1.glucocorticoid
a) hydrocortisone: acute
b) prednisolone: long term
c) dexamethasone: short term
2.mineralcorticoid
a) fludrocortisone: short acting
b) aldosterone

24
Q

nl1

NSAIDS

A
  1. non-selective COX inhibitor
    aspirin: low dose antiplatelet coz irreversibly inhibit PLT/COX1. mid dose analgesic & antipyretic coz prevent PGE2 release. high dose anti-inflammatory.

uses: post MI, post stroke. *Reye’s syndrome if given in children with viral infxn

ibuprofen, diclofenac, indomethacin
2. selective COX-2 inhibitor
celecoxib: inhibit COX2 without inhibiting COX1. less gastric mucosal damage compared to non-selective COX inhibitor. *increase risk of MI/stroke

uses: pt with high risk of GI bleeds

25
Q

nl1

drugs for gout

A
  1. acute gout
    -corticosteroids
    -NSAIDS (naproxen, indomethacin)
    -colchicine: inhibit release of acids from phagocytes into joints. [also used in chronic gout, preferred in pt who cannot tolerate NSAIDs eg GI ulcers]
  2. chronic gout
    -allopurinol: inhibit XO enzyme [CI in acute gout]
    -probenecid (uricosuric med): increase renal elimination of uric acid, inhibit reabsorption of uric acid in PCT [increase fluids if taking this]
    -rasburicase: converts uric acid to allantoin which is a highly soluble compound [CI in G6PD]
26
Q

nl1

drugs for RA

A
  1. corticosteroids
  2. NSAIDS
  3. biologics (DMARD-slow progression of ds by acting on immune cells to prevent inflammatory cascade)
    -etanercept,infliximab: TNF alpha antagonist.
    -anakinra: IL-1 antagonist
  4. non-biologics (DMARD)
    -methotrexate: directly inhibit proliferation, stimulate apoptosis in immune-inflammatory cells
    -azathioprine: inhibit T cell activation and proliferation
27
Q

nl1

drugs for OA

A

acetaminophen and oral NSAID

28
Q

nl1

antiepileptics

A

1.Older
-phenytoin: inhibit voltage gated Na channel, prolongs duration of inactivated state, reduce activation, decrease release of glutamate, low neuronal excitability. 1st line for partial seizures, trigeminal neuralgia. Zero order kinetics. Narrow therapeutic index and enzyme inducer.
-carbamazepine: inhibit voltage gated Na channel. Tx partial seizures, trigeminal neuralgia.
-valproic acid: inhibit VGSC. inhibit T type Ca channel. broad spectrum antiepileptic. cause spina bifida.
-ethosuximide: inhibit T type Ca channel. Tx for absence seizure/petit mal.
-phenobarbitone: prolong duration of opening of Cl channel
-benzodiazepine: increase freq of Cl channel opening. 1st line for status epilepticus. diazepam is preferred in febrile seizures. clonazepam in absence seizure.

  1. newer
    -gabapentin: inhibit N type Ca channel, increase release of Gaba, decrease glutamate
    -lamotrigine: inhibit VGSC and N type Ca channel. preferred for generalised tonic clonic in repro age grp
    -vigabatrin: inhibit gaba transaminase, increase gaba
    -tiagabine: inhibit gaba uptake transporter, increase gaba at gaba R
29
Q

nl1

cavities and its struc

A

Optic canal: optic nerve, ophthalmic artery
SOF: CN3, 4, 6, V1
Foramen rotundum: V2
Foramen ovale “think of MALE”: V3, accessory meningeal artery, lesser petrosal nerve, emissary vein
Foramen spinosum: middle meningeal artery
IAM: CN 7,8
Jugular foramen: CN9, 10, 11, IJV

30
Q

ag1

drugs for DM T2

A

1.insulin secretagogues
-glyburide (sulphonylurea): stimulate insulin containing vesicles to release more insulin
-repaglinide (meglitinide):stimulate insulin containing vesicles to release more insulin. take before meal

2.insulin sensitiser
-metformin ( biguanide): inhibit hepatic gluconeogenesis, increase peripheral glucose uptake, increase glycolysis. AE is lactic acidosis
-rosiglitazone (TZD): binds to PPAR-gamma, increase expression of GLUT4, more glucose uptake. CI in HF
-acarbose (alpha-glucosidase inhibitor): decrease postprandial glucose. inhibits intestinal membranne alpha-glucosidases, inhibit glucose absoprion

3.others
-dapagliflozin (SGLT inhibitor): blocks SGLT-2, prevent reabsorption of glucose at PCT. AE: UTI
-sitagliptin (DPP-4 inhibitor) &** exenatide** (GLP-1 agonist): increase insulin secretion and reduce appetite. AE:pancreatitis
-pramlintide: reduce appetite/weight loss. reduces postprandial glucagon secretion.

31
Q

nl2

cerebrovascular accidents (ischaemic and hemorrhagic)

A

pathophysiology and histology:
1. 1 hr: failure of ATP-gated ion channels. minimal changes +cytotoxic edema.
2. 12-24h: activity and dissolution of Nissl bodies. Red neurons+pyknotic nuclei
3. 1-3D: neutrophilic invasion w/ disruption of tight junc of BBB. liquefactive necrosis+neutrophils+vasogenic edema
4. 3-7D: macrophage & microglial invasion
5. 1-2W: reactive gliosis. Astrocyte proliferation, glial hypertrophy and vascular proliferation at peripheral sites of necrosis
6. >2W: dense astrocytic processes surrounding cavity of necrotic debris.** cystic spaces surrounded by glial scarring**

FPE 1 (1 decks)

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