last minute Flashcards
stroke volume
stroke volume = EDV- ESV
end diastolic volume
end systolic volume
ejection fraction =
EJ= stroke volume ( end diastolic volume- end systolic volume) /end distolic volume
stroke volume= end diastolic volume- end systolic volume
e.g.
120- 80/120= 33%
Naloxone is a
competitive antagonist, non-selective for all opioid receptors.
4) A 69 year female with atrial fibrillation reports no episodes of palpitations and does not have any other cardiovascular disease. Which antiarrhythmic agent would you prescribe to control rate for this patient?
A. Flecainide
B. Bisoprolol
C. Amiodarone
D. Digoxin
E. Ivabradine
Answer is B. Bisoprolol beta blocker for rate control. Flecainide would be appropriate for rhythm control as would amiodarone (possible for rate if beta blocker and CCB contraindicated).
10) A 36 year female has been admitted to a general ward with a severe infection. She has been prescribed i.v. antibiotics. A steady state plasma concentration is reached in 5 hours. What would be the predicted half-life of the antibiotic?
A. 10 hours B. 25 hours C. 1 hour
D. 15 hours E. 7.5 hours
The answer is C. 1 hour. Css should be reached in approximately 5 half-lives. 5/5=1.
ADR reactions
11) A junior doctor is reviewing the medications of an elderly patient. The patient reports that they have stopped taking one of their medications because it was causing side effects they describe as shaking or tremor. The doctor ascertains that it is a type B adverse drug reaction and goes about reporting it to the Medicines and Healthcare products Regulatory Agency through the online yellow card system. Which of the below does not describe a type B ADR?
A. Dose-related
B. Uncommon
C. Unpredictable
D. Serious/irreversible
E. Associated with high mortality
A. Dose-related
In patients with resistant hypertension, who have been prescribed drugs in accordance with guidelines up to and including step three, additional add on drugs can be prescribed. Name ONE class of drug (excluding a diuretic) that may be considered. Provide an example from this class and briefly describe how it lowers blood pressure.
Alpha blocker (1 mark), doxazosin (1 mark) cause vasodilation reducing the PVR (1 mark)
OR
Beta blocker – beta adrenergic receptor antagonist (1 mark), labetalol, bisoprolol, metoprolol (1 mark) lower renin levels, negative chronotropic and inotropic effects, decreased cardiac output
What clinical marker will the doctor measure to access how well her diabetes is being controlled and what target (%) would they be hoping for?
HbA1c (1 mark) 6.5% in first two treatment steps (1 mark)
DM diagnosis parameters
Fasting glucose >6.9 mml/L
Random plasma glucose >11 mmol/L
HbA1C >48 mmol/mol
A single raised plasma glucose without symptoms not sufficient for diagnosis ( would need several blood tests in the absence of symptoms)
Plasma or urine ketones
She is currently taking metformin TDS. How does metformin help control her diabetes?
Decrease insulin resistance (sensitivity of own insulin), (1 mark) increasing glucose uptake and utilisation in target tissues (skeletal muscle) (1 mark). Reduces hepatic glucose production. (Limits weight gain) (1 mark).
One of the participants in the phase 0 trial, develops breast cancer aged 55 (unrelated to the trial). Name the type of hormone replacement therapy (HRT) that increases the risk of breast cancer when used in the short term. Provide an example drug from this class.
Opposed oestrogen therapy (1 mark)
- oestrogen needs to be opposed by progesterone to prevent breast cancer
Estradiol with medroxyprogesterone, .
Specific dose combinations and trade names do not need to be learnt. (1 mark)
(Longer term unopposed HRT can increase risk of breast cancer and is suggested to be associated with increased age and other risk factors.)
Tamoxifen is discussed as an appropriate chemotherapeutic agent. What does this information suggest about the breast cancer diagnosis and to what class of chemotherapies does it belong?
Oestrogen receptor positive (1 mark) SERM (1 mark)
stages of kidney
pronephros (cervical region)
mesonephros (embryonic kidney)
Metanephros- true/definitive kidney
Ureteric bud (sprouts of the mesonephric duct) induces development of
the definitive kidney
Ureteric bud induces the development of the true kidney–> from the metanephros tissue
what happens to the metanephric kidney after it appears in the pelvic region
it ascends!!!
Kidney and gonad undergo apposing changes
- Gonad descends
- Kidney ascends–> moves up through embryonic body due to expansion of the cavity
Renal agenesis (no kidney)
Ureteric bud fails to interact with intermediate mesoderm
Structural anomalies related to migration
pelvic kidney- doesnt ascend properly
horseshoe kidney- 2 developing true kidneys move up through the abdominal cavity together due to the caudal poles fusing –> limits migration e.g. first unpaired branch of the abdominal aorta–> doesn’t cause too many symptom
Symptomatic consequence is ectopic ureteral opening
- Openings can be anywhere from the bladder, the vagina
- Into the urethra (no muscular or sphinctal control of bladder)
- Symptoms- incontinence –> doesn’t pass through bladder for storage phase
*
urorectal septum divides
the cloacal membrane into two membranes: the urogenital membrane (ventrally) and the anal membrane (dorsally).
development in the urinary tracts in females
(XX)
- Mesonephric ducts (MD) reach urogenital sinus (UGS)
- Ureteric bud sprouts from MD
- Urogenital sinus begins to expand
- Mesonephric duct regresses à no testosterone (XX)
- Ureteric buds open into the urogenital sinus
development of the urinary tract in males
- Mesonephric ducts (MD) reach urogenital sinus (USG)
- Ureteric bud sprouts from MD
- Smooth musculature begins to appear and UGS begins to expand
- Ureteric bud and Mesonephric Ducts make independent openings in UGS
- Due to presence of androgen (testosterone)
- MD become converted into the vas deferens
- Then the prostate and prostatic urethra forms
male urethra divided into 4 parts
Pre-prostatic
Prostatic
Membranous- through the perineum
Spongy – external genitalia under influence of androgens
development of male urethra
In the male the Genital tubercle elongates and genital folds fuse to form spongy urethra
storage is a
sympathetic process
- hypogastric nerveprevents contraction of the detrusor (B3) whilst causing contraction of the IES (alpha1)
testosterone treated women
- Exogenous androgen
- Supports wolffian duct
- But no testis- therefore no MIH
- Therefore mullerian ducts develops
androgen insensitive male
Androgen Insensitivity Syndrome
Receptors for testosterone don’t work
Wolffian ducts don’t survive
But MIH present so Mullerian ducts degenerate
external indifferent stage
Genital tubercle (FT)
Genital folds
Genital swelling
External genitalia – male
In male the genital tubercle elongates and genital folds fuse to form the spongy urethra
GT develops into glans penis
Influence of testis- derived androgen hormones- dihydrotestosterone
External genitalia – female
No fusion occurs in the female
Development of labia majora and labia minora
Genital tubercles develops into clitoris
Urethra opens into the vestibule
reversed rotation: midgut development problem
1 x 90 degrees rotation clockwise
Transverse colon behind the SI
summarise Ph A1 cartilage
mechels cartilage
Maxillary cartilage (first bump)
- Gives rise to incus
Meckel’s cartilage (second bump)Mandible cartilage
- Gives rise to malleus
- trigmeninal nerve associated- muscles of mastication*
summarise Ph A2
Reichert’s
- Stapes
- top of hyoid
facial nerve- muscles of facial expression
biochemist studying the function of the enzyme glucokinase fits a graph of experimental data using the Michaelis-Menten equation.
Which option represents this equation ?
C
fracture types
