revision Flashcards
ag3
antifungal: amphotericin B & nystatin
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
ag3
antifungal: ketoconazole, fluconazole, itraconazole
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
ag3
antifungal: terbinafine
MOA: inhibit squalene epoxidase, inhibit synthesis of ergosterol
ag3
antifungal: caspofungin (echinocandin)
MOA: inhibit 1,3-beta glucan synthase, depletion of beta-glucan polymers, block cell wall synthesis
ag3
antifungal:
flucytosine
griseofulvin
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
ag3
oxytoxic: oxytocin
MOA: bind to G protein coupled oxytoxic receptors on uterine smooth muscle cells, release IP3, increase intracellular Ca, uterine contractions
Uses: INDUCTION OF LABOUR
ag3
oxytoxic:ergometrine
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.
ag3
oxytoxic:
mifeprostone
misoprostol (PGE1)
dinoprostone (PGE2)
carboprost (PGF 2 alpha)
-mifeprostone: terminate pregnancy
-misoprostol, dinoprostone, carboprost promote cervical ripening/cervical softening + thining and dilation of cervix= facilitate labour
*carboprost for postpartum hemorrhage
ag3
tocolytic:
nifedipine (CCB)-tachycardia, HoTN
atosiban (oxytocin R antagonist)
ritodrine (beta 2 agonist)-tremors
salbutamol (beta 2 agonist)-tremors
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
ag3
OCP:
-oestrogen+progesterone (monophasic, diphasic, triphasic)
-minipills/progesterone only
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
ag3
post coital pill: levonorgestrel (emergency)
injectable progestin: medroxyprogesterone acetate
-levonorgestrel: release progesterone, cervical mucus & endometrium effect
-medroxyprogesterone acetate: supress ovulation and thicken cervical mucus in high levels of progestin
ag3
selective oestrogen receptor modulators:
clomiphene (antagonist at hypothalamus=increase GnRH)
tamoxifen (antagonist at breast)
raloxifene (agonist at bone)
clomiphene: treat infertility
tamoxifen: breast cancer
raloxifene: tx osteoporosis
ag3
nocturnal pulsatile secretion of GnRH brings on puberty
in girls which develop first? in boys?
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
ag2
anti-herpes
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)
ag2
anti-hepatitis
HBV: interferon alpha, tenofovir, lamivudine
HCV: ribavirin, ledipascir, sofosbuvir
ag1
pancreatic carcinoma
*endocrine cells (islet of Langerhands) mostly at tail 20%
exocrine 80%
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
ag1
types of colitis
1. Ulcerative colitis and Crohn’s disease
2. pseudomembranous colitis
3. infective (Amoebic, TB)
4. Ischaemic & radiation
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)
ag1
drugs for peptic ulcers
- 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 - 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 - Anticholinergics
-pirenzepine: block muscarinic M1 receptor on parietal cells, inhibit gastric acid secretion - 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] - 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]
ag1
triple and quadriple therapy for H. pylori
triple therapy: OCLAM
omeprazole-increase stomach pH, antimicrobial
clarithromycin
amoxicillin/change to metro if allergic
quadraple therapy: OBMT
omeprazole
bismuth
metronidazole
tetracycline
ag1
drugs for IBD (crohns and UC)
- 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 - 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
ag1
drugs for GI infestations
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
nl1
back muscles
- splenius
-splenius capitis
-splenius cervicis - erector spinae (ILS)
-iliocostalis m.
-longissimus m.
-spinalis - transversospinalis m.
-semispinalis
-rotators
-multifidus - suboccipital (got suboccipital triangle which vertebral artery passes through
-4 muscles
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
1.glucocorticoid
a) hydrocortisone: acute
b) prednisolone: long term
c) dexamethasone: short term
2.mineralcorticoid
a) fludrocortisone: short acting
b) aldosterone
nl1
NSAIDS
- 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
