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1
Q

stroke volume

A

stroke volume = EDV- ESV

end diastolic volume

end systolic volume

2
Q

ejection fraction =

A

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%

3
Q

Naloxone is a

A

competitive antagonist, non-selective for all opioid receptors.

4
Q

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

A

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).

5
Q

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

A

The answer is C. 1 hour. Css should be reached in approximately 5 half-lives. 5/5=1.

6
Q

ADR reactions

A
7
Q

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

A. Dose-related

8
Q

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.

A

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

9
Q

What clinical marker will the doctor measure to access how well her diabetes is being controlled and what target (%) would they be hoping for?

A

HbA1c (1 mark) 6.5% in first two treatment steps (1 mark)

10
Q

DM diagnosis parameters

A

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

11
Q

She is currently taking metformin TDS. How does metformin help control her diabetes?

A

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).

12
Q

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.

A

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.)

13
Q

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?

A

Oestrogen receptor positive (1 mark) SERM (1 mark)

14
Q

stages of kidney

A

pronephros (cervical region)

mesonephros (embryonic kidney)

Metanephros- true/definitive kidney

15
Q

Ureteric bud (sprouts of the mesonephric duct) induces development of

A

the definitive kidney

Ureteric bud induces the development of the true kidney–> from the metanephros tissue

16
Q

what happens to the metanephric kidney after it appears in the pelvic region

A

it ascends!!!

17
Q

Kidney and gonad undergo apposing changes

A
  • Gonad descends
  • Kidney ascends–> moves up through embryonic body due to expansion of the cavity
18
Q

Renal agenesis (no kidney)

A

Ureteric bud fails to interact with intermediate mesoderm

19
Q

Structural anomalies related to migration

A

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

20
Q

Symptomatic consequence is ectopic ureteral opening

A
  • 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
    *
21
Q

urorectal septum divides

A

the cloacal membrane into two membranes: the urogenital membrane (ventrally) and the anal membrane (dorsally).

22
Q

development in the urinary tracts in females

A

(XX)

  1. Mesonephric ducts (MD) reach urogenital sinus (UGS)
  2. Ureteric bud sprouts from MD
  3. Urogenital sinus begins to expand
  4. Mesonephric duct regresses à no testosterone (XX)
  5. Ureteric buds open into the urogenital sinus
23
Q

development of the urinary tract in males

A
  • 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
24
Q

male urethra divided into 4 parts

A

Pre-prostatic

Prostatic

Membranous- through the perineum

Spongy – external genitalia under influence of androgens

25
Q

development of male urethra

A

In the male the Genital tubercle elongates and genital folds fuse to form spongy urethra

26
Q

Nephrotic syndrome

A

e.g. diabetic nephropathy’s, minimal change disease and membranous glomerulonephritis, focal segmental glomerosclerosis (FSGS)

  • Proteinuria (typically >3g/d) sufficient to cause
    • Hypalbuminaemia
    • Sufficient to cause:
      • Oedema

treatment- blood pressure control

27
Q

diabetic nephropathy treatment

A
  • Hypertension
  • Good glycaemic control
  • ACE inhibitors
  • Angiotensin receptors blockers
28
Q

nephritic syndrome

A

e.g. IgA nephropathy (Berger Disease), rapidly progressive glomerulonephritis, post-streptococcal glomerulonephritis, good pastures syndrome

  • Oliguria- no urine output
  • Hypertension
  • Hematuria – microscopic or macroscopic
29
Q

pathology of nephritic syndrome

A
  • Inflammation that disturbs basement membrane
  • Bigger gaps in basement membrane
  • RBC can pass through into the urine
  • Haematuria – coke coloured urine
30
Q

pathology of nephrotic

A
  • Damage to podocytes–> large amounts of protein being lost in urine e.g. albumin
    • O of nephrotic links to oedema
    • Reduction of albumin in the body – lost in urine
    • Less oncotic pressure
31
Q

voiding is a

A

parasympathetic process

- pelvic nerve (M3) stimulated–> detrusor muscle contraction

  • pudendal nerve inhibited (nicotinic ACh)–> relaxation of EUS
32
Q

storage is a

A

sympathetic process

  • hypogastric nerveprevents contraction of the detrusor (B3) whilst causing contraction of the IES (alpha1)
33
Q

mesoderm made up of

A

Paraxial mesoderm turns into somites

  • Skeletal muscle
  • Vertebra
  • Cartilage

Intermediate mesoderm

  • Kidneys and gonads

Lateral plate mesoderm

  • Somatic – body walls
  • Splanchnic – visceral

Ectoderm

  • Epidermis (nails, skin etc)
  • Nerve tissue
34
Q

……….mesoderm on both side of the embryo condenses into 2

A

intermediateurogenital ridges

  • runs parallel to the the future vertebral column
  • organises into a cylinder of mesoderm called the nephrogenic cord
35
Q

indifferent stage: a pair of duct

A
  • Mesonephric ducts develop in both male and female embryos
  • Paramesonephric ducts develop in both male and female embryos
  • Both the mesonephric and paramesonephric ducts end at the urogenital sinus part of the cloaca
    • Mesonephric ducts is also known as Wolffian duct
    • Paramesonephric duct is also know as the Mullerian duct
36
Q

mesonephric duct

A

wolffian duct- male

37
Q

paramesonephric duct

A

mullerian duct- female

38
Q

male reproductive system

A

sex determining gene carried on Y chromosome

  • testosterone produced which maintains the mesonephric duct (wolffian duct)
  • mullerian inhibiting factor produced- paramesonpheric duct regresses
39
Q

female reproductive system

A

no testosteorne produced- mesonephric ducts disintegrate

no MIH produced - paramesonephric (mullerian) ducts maintained

40
Q

testosterone treated women

A
  • Exogenous androgen
  • Supports wolffian duct
  • But no testis- therefore no MIH
  • Therefore mullerian ducts develops
41
Q

androgen insensitive male

A

Androgen Insensitivity Syndrome

Receptors for testosterone don’t work

Wolffian ducts don’t survive

But MIH present so Mullerian ducts degenerate

42
Q

Development of the ductal systems- summary

A
  • Mesonephric duct functions in both male and female embryos as duct of the embryonic kidney
  • Paramesonephric (Mullerian) ducts appear in both
  • Mesonephric duct ceases to be of use to the urinary system and will degenerate unless testis-derived testosterone is present- wolffian pathway
  • Paramesonephric duct regresses in the present of testis-derived MIH
43
Q

external indifferent stage

A

Genital tubercle (FT)

Genital folds

Genital swelling

44
Q

External genitalia – male

A

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

45
Q

External genitalia – female

A

No fusion occurs in the female

Development of labia majora and labia minora

Genital tubercles develops into clitoris

Urethra opens into the vestibule

46
Q

colon should be on the …….. hand side

A

right

47
Q

small intestine should be on the

A

left hand side

48
Q

reversed rotation: midgut development problem

A

1 x 90 degrees rotation clockwise

Transverse colon behind the SI

49
Q

omphalocele

A
  • When the herniation fails to return to the abdominal cavity in week 10
  • Herniated contents still remain within the umbilical cord
  • Midgut structures still covered with peroneal covering
    • Not exposed to amniotic fluid
  • Mortality is high due to other developmental abnormalities
50
Q

gastroshisis

A

midgut development problem

  • Failure of abdominal wall to form anteriorly due to incomplete lateral folding
  • Defect in abdominal wall through which abdominal viscera can permeate
  • Not covered in peritoneum
  • Exposed to amniotic fluid
  • Negatively effects gut development
  • May not fit in abdominal cavity
  • Fewer developmental defect than omphalocele so mortality rate lower
51
Q

urorectal septum

A
  • descends caudally, separates the cloaca into an anterior urogenital and a posterior anorectal space
  • urogenital space is a wedge of mesoderm that continues to descend until we have completely separated urogenital and anorectal spaces
52
Q

summarise Ph A1 cartilage

A

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*
53
Q

summarise Ph A2

A

Reichert’s

  • Stapes
  • top of hyoid

facial nerve- muscles of facial expression

54
Q

summarise Ph A3

A
  • remainder of the hyoid
  • glossopharnagel*
  • Stylopharangeus
  • internal carotid*
55
Q

summarise Ph A4

A

Cartilage of the larynx

Thyroid cartilage

  • vagus*
  • aorta*
  • Pharyngeal constrictors
  • Cricothyroid
56
Q

summarise PhA6

A

Cartilage of the larynx

  • vagus*
  • ​pulmonary arch*
57
Q

atorvostatin vs simvastin

A

atorvostatin –> first lines

simvastatin–> pushes towards DM but more effective

Simvastatin is a prodrug activated by first pass metabolism – t1/2 around 2h

  • taken at night

Atorvastatin is active- first pass metabolism- also active derivatives- t1/2 around 24h

58
Q

A 32 year old woman who has missed her last period has been feeling sick in the mornings, tired, and is needing to pass urine more often. The woman takes a pregnancy test which comes back positive.

Where does fertilisation of the ovum usually occur?

A

Ampulla region of a Fallopian Tube

Fertilisation of the ovum occurs within the fallopian tube.

Implantation of the fertilised ovum then occurs at the posterior uterine wall.

59
Q

biochemist studying the function of the enzyme glucokinase fits a graph of experimental data using the Michaelis-Menten equation.

Which option represents this equation ?

A

C

60
Q

Which term describes the distance between cells at the same stage of spermatogenesis down the length of the seminiferous tubule?

A

The spermatogenic wave.

Note: The Spermatogenic cycle is different from the spermatogenic wave and is defined as time taken for reappearance of the same stage within a given segment of tubule (~16 days in human).

61
Q

fracture types

A
62
Q

With respect to fatty acid catabolism, which enzyme facilitates the activation of fatty acids by linking coenzyme-A?

A

Fatty acyl CoA synthase.

63
Q

An electrophysiologist studying the function of the CFTR protein characterises the functional consequences of a gene mutation which results in a negatively charged amino acid being mutated to a positively charged amino acid.

Which mutation did the electrophysiologist characterise?

A

Glutamic acid (D) to Lysine (K)