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MD3002 > WEEK 5 > Flashcards

WEEK 5 Flashcards

1
Q

What are the 6 causes of hepatitis?

A
  1. Viral
  2. Non-viral
  3. Drugs - paracetamol
  4. Alcohol
  5. Poisons - aflatoxins
  6. Other e.g. pregnancy, circulatory insufficiency
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2
Q

Define hepatotropic.

A

All demonstrate an ability to infect hepatocytes

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3
Q

What are the 6 stages of viral replication?

A
  1. Adsorption
  2. Penetration
  3. Uncoating
  4. Replication of nucleic acid
  5. Maturation/assembly
  6. Release
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4
Q

What are the viral feautre of hepatitis A?

A
  • single stranded RNA virus that is non-enveloped (naked)

- has only 1 serotype

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5
Q

How is hep A spread/transmitted? (HINT: there’s 3 routes)

A

Faecal-oral
Poor hand hygiene
Contaminated food or water

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6
Q

What are the stages of infection for HAV?

A
  1. Incubation period of 2-4 weeks (prodromal phase)
  2. Virus excreted in faeces for 1-2 weeks before symptoms
  3. Translocation from GI tract to blood
  4. Infection of liver cells
  5. Passage to biliary tract and back to GI
  6. Excretion in faeces
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7
Q

What are the clinical features of HAV? How is HAV diagnosed?

A

Fever, anorexia, nausea, vomiting, jaundice, dark urine, pale stools
- liver moderately enlarged, spleen palpable in 10% pts
Diagnosed by presence of anti-HAV

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8
Q

What is the current treatment used for HAV? How is HAV prevented?

A

No specific treatment
- maintain comfort and nutritional balance
- fluid and electrolyte replacement
PREVENTION = vaccine, good hygiene
- resistant to chlorination - killed by boiling for 10mins

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9
Q

What are the viral features of hepatitis B?

A
  • double stranded DNA virus

- enveloped virus

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10
Q

What are the 3 HBV antigens? Describe them.

A
  1. HBaAg = surface antigen
    - indicated high transmissibility
    - provides immunity and appears late
  2. HBcAg = core antigen
    - appears early in infection
  3. HBeAg = enveloped antigen
    - derived from core and indicates high infectivity
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11
Q

How is HBV transmitted/spread?

A

Sexual intercourse
Intra-uterine, peri- and post-natal infection
Blood or blood products
Contaminated needles and equipment used by IV drug users
Tattooing, body piercing and acupuncture
Contaminated haemodialysis equipment

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12
Q

What are the stages of infection of HBV?

A

Incubation period of 2-4 months

- 50% pts develop chronic active hepatitis = 20% lead to cirrhosis and 1-4% of these risk developing liver cancer

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13
Q

What are the stages of ACUTE infection of HBV?

A

Incubation period = 45 - 120 days

  • pre-icteric period of 1-7days
  • icteric period of 1-2 months
  • convalescent period of 2-3 months in 80-90% of adult cases
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14
Q

How do you discriminate between acute and chronic HBV infection?

A

HBsAg and HBeAg appear during incubation period

  • viral DNA becomes detectable
  • Antibodies to core antigen appear concomitantly with rise in liver transaminases
  • Antibodies to HBeAg and HBsAg only appear during convalescence (acute)
  • Continued presence of HBaAg and absence of antibodies to it indicate that infection has become chronic
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15
Q

What are the clinical features of the (i) pre-icteric (ii) icteric period of HBV infection?

A

(i) malaise, anorexia, nausea, pain in RUQ (tender liver)
(ii) yellow pigmentation of skin, sclera and other mucous membranes
- caused by hyperbilirubaemia

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16
Q

What are the clinical outcomes of an acute HBV infection? (HINT: there’s 3)

A
  1. Fulminant hepatitis
  2. Chronic hepatitis or asymptomatic carrier state
  3. Resolution of infection
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17
Q

What is the (i) treatment (ii) prevention for HBV?

A

(i) pegylated interferon (peginterferon)
- nucleoside analogues such as oral lamivudine
(ii) vaccination of 3 injections over 6 months
- HBV immunoglobulin
- blood screening, needle exchange programmes and sexual health education

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18
Q

What are the viral features of HCV?

A

Accounts for 90% of non A non B transfusion associated hepatitis cases

  • 6 virus types
  • single stranded RNA that is enveloped
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19
Q

What are the clinical features of HCV infection?

A

Usually asymptomatic
- fatigue, nausea, weight loss, may rarely progress to cirrhosis, small proportion of pts develop hepatocellular carcinoma many years after primary infection

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20
Q

What are the ways in which HCV is transmitted?

A
  1. Blood and blood products
  2. Blood contaminated needles
  3. Tatooing, body piercing, acupuncture
  4. Haemodialysis
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21
Q

What are the (i) stages of infection (ii) screening for HCV?

A

(i) replicates mainly in hepatocytes and has incubation period of 2 weeks to 6 months
(ii) blood test available based on NAAT but hte current incidence of tranfusion - associated HCV is lowe

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22
Q

What is the current treatment for HCV infections?

A 
Ribavirin plus a pegylated alpha-interferon 
Combination therapy
- sofosbuvir (nucleotide analogue)
- boceprevir (protease inhibitor) 
- telaprivir (nuceloside analogue)
- Daclatasvir (inhibits NS5A)
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23
Q

What are the viral features of hepatitis D (delta)?

A

Small circular single-stranded RNA virus

  • defective virus
  • it picks up HBsAg as it buds from liver cell
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24
Q

When is HDV usually found? How is it transmitted? Who is at risk for infection? What is the current treatment?

A

Found as co-infection with HBV

  • transmitted percutaneously, sexually, from infected blood
  • chronic HBV carrier at risk of HDV infection
  • no specific treatment available
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25
Q

What are the viral features of Hepatitis E?

A

Caliciviridae

- single stranded RNA with a non-enveloped virus

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26
Q

What is the (i) transmission (ii) symptoms of HEV?

A

(i) waterborne disease with a peak incidence in young adults
(ii) can be life threatening in pregnant women
- signs and symptoms similar to other acute forms of hepatitis

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27
Q

How is HEV prevented? (HINT there’s 2 points)

A
  1. Good sanitation and hygiene

2. Vaccine (Hecolin)

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28
Q

What are the 6 other causes of viral hepatitis?

A 
Epstein-Barr virus
Cytomegalovirus
Yellow fever virus
Adenoviruses
Bunyaviruses
Flaviviruses
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29
Q

What are the 4 types of hosts for helminthic infections?

A
  1. Definitive
  2. Intermediate
  3. Accidental
  4. Paratenic
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30
Q

What are the 4 types of vectors for helminthic infections?

A
  1. FLIES = onchocerciasis
  2. AEDES MOSQUITO = filariasis
  3. CRYSOPS = guinea worm
  4. SNAILS = schistosomiasis, capillaria, fasciola
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31
Q

Name 6 examples of helminth infections where inflammation is the main pathogenic mechanism.

A
  1. Filariasis
  2. Onchocerciasis
  3. Toxocariasis
  4. Cysticerosis
  5. Chostosomiasis
  6. Enterobius
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32
Q

What are the 4 types of pathological mechanisms for helminth infections?

A
  1. Inflammation
  2. Competition for nutrients
  3. Space occupying lesions
  4. Stimulation of fibrosis
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33
Q

What are the clinical features of trichiuris?

A

Vague abdominal symptoms, dysentry syndrome

  • growth retardation
  • intellectual comrpomise (micronutrient deficiency, mucosal integrity)
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34
Q

What are the clinical features of hookworm?

A
  1. Anaemia - each adult hookworm takes up to 0.4mL blood

2. Vague abdominal pain

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35
Q

What are the clinical features of ascaris?

A
  1. Vague abdominal pain
  2. Intestinal pain
  3. Hepatobiliary obstruction and jaundice
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36
Q

What does (i) lung fibrosis (ii) liver fibrosis (iii) bladder fibrosis result in?

A

(i) RHF
(ii) portal hypertension
(iii) bladder cancer

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37
Q

What is the approach to the treatment of helminth infections?

A

It differs depending on the pathogenesis

(1) INFLAMMATION = anti-inflammatory e.g. steroids
(2) COMPETITION FOR NUTRIENTS = reduce worm burden and support nutrition
(3) SPACE OCCUPYING LESIONS = surgery, decompression
(4) STIMULATION OF FIBROSIS = helminth eradication and treatment of secondary effects

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38
Q

What drug(s) are used to treat (i) cestodes (ii) nematodes?

A

(i) Praziquantel but remember the problems of cysticerosis where it’s necessary to continue anti-epileptic drugs and combine anti-helminthic treatment w. steroids
(ii) Albendazole = most effective. Levamisole and piperazine rarely used. A single dose/course of treatment rarely enough as you must engage with fam and enviro

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39
Q

What is the MoA of praziquantel? What is it used to treat?

A

MoA not fully known but it probably increases calcium permeability of membranes depolarising them (and may interfere with purine synthesis)
TREATS: hydatid disease, cysticercosis, schistosomiasis, clonochic, fascioliasis and paragnomiasis infection

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40
Q

What side effects can praziquantel lead to?

A

Diziness, headache, drowsiness and somnolescence

  • abdo cramps, nausea and diarrhoea
  • transient asymptomatic rise in transaminases
  • urticaria, rash and pruritis
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41
Q

What is the MoA of albendazole? What is it used to treat?

A 
MoA = binds to colchicine sensitive receptor or tubulin which prevents polymerisation into microtubules. Impaired glucose uptake and degenerative changes appear in the worm
TREATS = nematode infections, some protozoa (giardia), some cestode (neurocysticercosis and hydatid disease)
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42
Q

What side effects can Albendazole cause?

A

Persistent sore throat

  • headaches, dizziness and seizures
  • acute liver failure
  • aplastic anaemia and marrow supression
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43
Q

What is the (i) MoA (ii) use of treatment (iii) side effects of Piperazine?

A

(i) active against gamma butyric acid receptor paralysing muscular activity
(ii) ascariasis and enterobius infection
(ii) GI tract upset and rarely hypersensitivity, dizziness

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44
Q

What is pyrantel used to treat? What does it cause?What is a risk associated with its use?

A

Treats hook and roundworms

  • causes depolarising NM blockade
  • can cause intestinal obstruction if there’s a heavy worm load
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45
Q

What is levamisoles MoA? What is it used to treat? What are its side effects?

A

Nicotinic ACh receptor antagonist used to treat ascariasis and mixed ascaris hookworm infection
SE = abdo pain, nausea and vomiting

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46
Q

How is the coelom formed?

A

The lateral plate mesoderm cavitates to form the coelom

- folding moves the intermediate mesoderm to the posterior abdominal wall while the coelom becomes the peritoneal cavity

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47
Q

What forms the urinary and reproductive systems?

A

Mesoderm and coelomic epithelium of the posterior abdominal wall. As well as the endodermally derived cloaca (divided by urorectal septum) and the allantois

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48
Q

How do the renal primordia form? Name the 3.

A

They form sequentially 3 times within the mesoderm of the posterior abdominal and pelvic walls
PRONEPHROS, MESONEPHROS and METANEPHROS
- the pronephros is non-functional but by eek 4 the mesonephros drains into the mesonephric duct

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49
Q

What do the mesonephric ducts open in to?

A

The cloaca
- which is being divided by the urorectal septum into the urogenital sinus and allantois anteriorly, with the recto-anal region posteriorly

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50
Q

What has happened by the 5th week with regards to the ureteric bud?

A

The ureteric bud (on each side) extends from the mesonephric (Wolffian) duct and induces the metanephros that is forming in the pelvis and will become the definitive kidney

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51
Q

Where do the metanephric blastema lie? What will they become?

A

Adjacent to each other

- become the kidneys

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52
Q

What does the ureteric bud give rise to?

A

The ureter and collecting ducts

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53
Q

What does metanephros become?

A

The renal tissue

- i.e.e glomeruli and loops of Henle

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54
Q

By what week is the kidneys functional?

A

About 10 weeks

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55
Q

What occurs if the collecting ducts don’t meet the nephric vessels?

A

CYSTS form within the kidney

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56
Q

What are the abnormalities that can arise during development of the kidneys?

A
  1. Pelvic Kidney (one of the kidneys lies within the pelvis)

2. Horseshoe kidney (kidneys are still connected and lie in pelvis)

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57
Q

What abnormalities can arise in ureteric development?

A
  1. Bifid ureter (if bud branches abnormally before it reaches the metanephric blastema)
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58
Q

What happens if the ureteric bud fails to branch at all within the metanephros?

A

There will be no induction of kidney development

- renal agenesis

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59
Q

What does the urogenital sinus form? How does this occur?

A

The bladder and urethra

  • the sinus grows and mesonephric ducts and ureteric buds (ureters) become incorporated w/in its walls
  • the mesonephric ducts move caudally to open in the urethra as the vas deferens and ejaculatory ducts
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60
Q

During weeks 4-6, what happens to the cloacal membrane?

A

The membrane ‘sinks’ in to a pit of ectoderm as the underling mesoderm proliferates

  • the urorectal septum completely separates the cloaca and becomes the perineal body
  • the cloacal membrane ruptures, leaving the anal canal and UG sinus open to the exterior; the roof of the UG sinus is the urethral plate
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61
Q

What do the following structures become; (i) proximal part of UG sinus (ii) allantois (iii) pelvic part of UG sinus (iv) distal part of endodermal UG sinus?

A

(i) bladder
(ii) closes to become urachus
(iii) prostatic and membranous urethrae
(iv) drawn along the floor of the extending genital tubercle as the urethral plate

62
Q

In summary, what 4 structures form the urinary system?

A

Metanephros
Ureteric bud
Urogenital sinus
Allantois

63
Q

What happens during week 6 of genito-urinary development?

A

The paramesonephric duct develops lateral to the mesonephric duct as an invagination from a cord of coelomic epithelial cells
- the mesonephric and paramesonephric ducts form the reproductive ducts and structures, while the gonad is formed in the mesoderm of genital ridge - which is developed from overlying coelomic epithelium and germ cells that have migrated from the yolk sac endoderm

64
Q

When is sexual differentiation seen?

A

From week 8 through to week 12

65
Q

What leads to female development?

A

An absence of the Y chromosome and SRY gene leads to female development from the paramesonephric ducts, whilst the mesonephric ducts degenerate (lack of testosterone)

66
Q

What is mesonephric remnants left in a female?

A

Gartner’s cysts near vagina or epoophoron and paroophoron near ovary

67
Q

What is the development like in males? What is the appendix epididymis?

A

Development from mesonephric ducts
- paramesonephric ducts degenerate but remain as the appendix testis and the prostatic utricle
APPENDIX EPIDIDYMIS = remnant of proximal end of mesonephric duct

68
Q

What are the 6 types of uterine abnormalities?

A
  1. Double uterus and double vagina
  2. Double uterus
  3. Bicornate uterus
  4. Separated uterus
  5. Unicornate uterus
  6. Cervical atresia
69
Q

Describe the development of the uterus and vagina, beginning with the 2 paramesonephric (Mullerian) ducts.

A

The 2 ducts meet in the midline and fuse with each other plus the sino-vaginal bulb (derived from posterior aspect of urogenital sinus)

  • during months 3-5 the ducts zip together in cranial direction to form proximal vagina and uterus
  • further cranially the ducts stay separate as L and R uterine tubes, with fimbriated ends that’re open to coelomic (peritoneal) cavity
  • as the ducts lift off of the posterior abdominal wall they lift peritoneum as the broad ligament
70
Q

How do the gonads remain ‘tethered’ to the surrounding mesoderm?

A

By the suspensory ligament and the gubernaculum that extends to the labioscrotal folds

71
Q

In females, the ovaries remain suspended from the broad ligament, but what happens in males?

A

The gubernaculum shrinks to draw the testis down the posterior abdominal wall to the inguinal canal, and then through the canal during months 8-9 and so should be in the scrotum by birth

72
Q

What is cryptochidism?

A

Failure of complete descent of testis into scrotum

- is common

73
Q

What happens to the gubernaculum in females?

A

It becomes the round ligament

  • the testis takes a loop of parietal peritoneum with it
  • the processus vaginalis that should remain only as the tunica vaginalis
74
Q

What happens if the *** stays open?

A

Indirect inguinal hernia

- hydrocele

75
Q

What does the urogenital sinus give rise to? What do these structures then form?

A

Rise to an endodermal urethral plate, genital tubercle, UG or urethreal folds, labioscrotal folds
FORM: external genitalia, growing into penis, penile urethra and scrotum in male; or remaining as the clitoris and the separate labia minora and majora in females

76
Q

In males, what happens to the urogenital/urethral folds in week 6?

A

The folds which form on either side of the urethral plate, fuse with the genital tubercle to grow with it and create the urethral groove between
- the folds and groove stop short of the end of the genetic tubercle (glans penis) but the urethral plate continues distally as a solid cord of (endodermal) cells

77
Q

How is the external meatus formed?

A

The cellular cord in the glans canalises, joins the penile urethra and forms the external meatus

78
Q

How is the penile urethra formed?

A

As the penis elongates, the edges of the urethral folds move towards each other and fuse in midline to create penile urethra
- the urethra ‘zips up’ from proximal to distal

79
Q

How is (i) Glans hypospadias (ii) penile hypospadias formed/arisen?

A

(i) abnormal canalisation of the urethra in the glans
(ii) failure of the urethral folds to form, or to extend along the penis and fuse throughout its full length (urethra opens on ventral surface of penis rather than on glans)

80
Q

What is the function of the renal system? (HINT: there’s 6 points)

A
  1. Regulation of ECF volume and BP
  2. Regulation of osmolality
  3. Maintenance of ion balance
  4. Regulation of pH
  5. Excretion of waste
  6. Production of hormones
81
Q

What are the main processes that occur in the nephron? (HINT: there’s 5 steps)

A
  1. Filtration by glomerulus
  2. Obligatory absorption and secretion by proximal tubule
  3. Generation of osmotic gradient by loop of Henle
  4. Regulated absorption and secretion by distal tubule
  5. Regulation of water uptake by collecting ducts
82
Q

Formation of filtrate occurs across a triple barrier, what are the 3 barriers?

A
  1. Endothelial lining of capillaries
  2. BM of capillaries
  3. Foot processes of epithelial cells (podocytes)
83
Q

What does the triple barrier do?

A

Allows free passage of solutes up to about 60kDa
Opposes movement of cells and large protein
Negatively charged molecule are filtered less easily than positively charged molecules

84
Q

What is (i) R.B.F (ii) R.P.F?

A

(i) the total amount of blood that traverses renal artery or vein per unit time (=1100ml/min)
(ii) total amount of plasma that traverses renal artery or vein per unit time

85
Q

If the haematocrit is 45% ad the RBF = 1100ml/min, what will the RPF be?

A

RPF = 55 x 1100

= 600ml/min

86
Q

What is the GRF?

A

Glomerular filtration rate = rate of filtrate production
- normal 125-130 ml/min when the size of the body has been corrected for (larger bodies have larger GFR, also GFR falls with age)

87
Q

What pressures (i) FAVOUR movement into tubule (ii) OPPOSE movement into tubule?

A 
(i) Hydrostatic of blood (+55mmHg)
Oncotic of tubule (0mmHg)
(ii) Hydrostatic of tubule (-15mmHg)
Oncotic of blood (-30mmHg)
BALANCE = 55 - 15 - 30 = +10 mmHg
88
Q

What are the autoregulation mechanisms for glomerular filtration?

A

Intrinsic or local control

  • myogenic mechanism
  • tubuloglomerular feedback (nephrogenic)
89
Q

Describe myogenic autoregulation.

A

Mediated by stretch receptors in arterioles
AFFERENT ARTERIOLE
(i) Constriction = reduces filtration rate, GFR falls
(ii) Dilation = increased pressure driving ultrafiltration, GFR increases
EFFERENT ARTERIOLE
(i) Constriction = causes pressure to back up w/in capillary, GRF increases
(ii) Dilation = allows blood to easily escape the capillary and pressure falls, GFR decreases

90
Q

Describe the renal blood flow?

A

1-1.2 L/min (20-23% of CO)

- is essentially constant over a wide range of BP (therefore GFR constant over wide range of BP)

91
Q

Describe tubuloglomerular feedback.

A

A function of the juxtamedulalry nephron

  • flow in distal convoluted tube is monitored and high flow info fed back to arterioles
  • in conditions of high filtrate flow in the tubule there’s an increase in Na and Ca conc. - these are monitored by macula densa cells adjacent to the DCT and a signal sent to afferent arteriole => constriction. Lowering flow rate to normal limits
92
Q

What extrinsic hormonal factors cause (i) decreased afferent blood flow (ii) increased afferent blood flow?

A 
(i) Symp nerve releasing norepinephrine
circulating epinephrine
Angiotensin II
(ii) renal prostaglandins
atrial natriuretic peptide
93
Q

What is (i) oesophageal stricture (ii) achalasia?

A

(i) narrowing or tightening of the oesophagus that causes swallowing difficulties
(ii) the muscles of the lower part of the oesophagus fail to relax, preventing food from passing into the stomach.

94
Q

Where do (i) squamous cell cancer (ii) adenocarcinomas commonly occur? (Name countries)

A

(i) China, Iran, Central Asia, Siberia, Mongolia, Afghanistan, Africa, Iceland and Finland
(ii) Western population

95
Q

What are the 3 important/prevalent causes of chronic liver disease?

A

Hepatitis B
Hepatitis C
Alcohol

96
Q

What is the difference in symptoms of diarrhoea due to (i) functional disease or (ii) organic disease?

A

(i) long standing, no diarrhoea at night

(ii) weight loss, fever, short duration

97
Q

How do you know whether it is diarrhoea of the (i) small-bowel or (ii) large-bowel?

A

(i) large volume, frothy, greasy, foul-smelling, undigested material
(ii) more than 6x day containing blood, mucus and/or pus, with tenesmus

98
Q

What symptoms would suggest diarrhoea is associated with malabsorption?

A

Bulky, frothy, greasy stool, undigested material

99
Q

What are the symptoms for an adult coeliac pt that’s (i) typical (ii) atypical?

A

(i) chronic diarrhoea

(ii) short statue, anaemia, metabolic bone disease and infertility

100
Q

What are the functions of the PCT (proximal convoluted tubule)?

A

Most of the recovery of ions, sugars, amino acids, peptides and a considerable amount of the total water is achieved in 1st part of PT
- in addition the PT actively secretes a no. of compounds for excretion with urine, and metabolises some of the amino acids

101
Q

How does resorption work? Mention the 2 pathways molecules and ions might take across the tubule epithelium.

A
  1. Transcellular route (through cell body)

2. Paracellular route (through leaky ‘tight’ junctions between cell bodies)

102
Q

What are the forces involved in the obligatory reabsorption from the proximal tubule? Give a summary (HINT: there’s 5 points)

A
  1. Ion gradients across basolateral membrane - active transport 3Na out 2K in
  2. This sets up an ECG of -3mV (tubule lumen neg causing paracellular efflux of cations)
  3. Osmotic gradient set up by pumping Na out cell into interstitial space
  4. Water moving along paracellular path due to osmotic pressure drags solutes along with it = solvent drag
  5. Chemical conc of solutes left behind when water leaves tubule facilitates a chemical gradient
103
Q

What is the transport maximum? What is its units? When can the transport max be exceeded?

A

There is limits as to ho much can be moved = Tm or Tmax

  • measured in mg/min or mmol/min
  • if blood conc is high it can be exceeded e.g. diabetes mellitus
104
Q

How is the amount filtered calculated? The threshold is equivalent to Tmax, what happens above this value?

A

Plasma conc (mg/ml) x GFR (ml/min)

  • substance will appear in urine
105
Q

What is the relationship between Tmax and secretion?

A

The amount filtered is proportional to the amount present in the plasma

  • plus, there’s addition of the substance from the blood TO to the tubule (secretion)
  • the amount appearing in the urine is the amount filtered plus the amount secreted
  • once max secretion level is reached, the secretion line levels off
106
Q

How are the followed solutes moved; (i) urea (ii) lipid-soluble substances (iii) phosphate (iv) protein?

A

(i) simple diffusion resorbs 50-60% and the rest is lost
(ii) simple diffusion
(iii) Na-linked transport
(iv) small amount digested to amino acids w/in tubule cells

107
Q

What are the % of obligatory resorption of (i) glucose, amino acids and lactate (ii) bicarbonate (iii) water and Na (iv) potassium (v) chloride

A

(i) 100%
(ii) 90%
(iii) 65%
(iv) 55%
(v) 50%

108
Q

What is clearance?

A

The clearance of any substance excreted by the kidney is the volume of plasma which is cleared of the substance per unit time (ml/min)
- it represents a theoretical volume of plasma cleared per min as in reality, no substance is completely cleared during its passage through the kidney

109
Q

What 3 renal processes determine and modify the composition of urine?

A
  1. Glomerular filtration
  2. Tubular reabsorption
  3. Tubular secretion
110
Q

What is the F.F.? How is it calculated?

A

The filtration Fraction

= GFR/RPF

111
Q

How is the renal clearance calculated?

A

To equate the urinary excretion rate of X to its renal arterial plasma conc (Pa) it’s necessary to determine the rate at which X is removed from plasma - the clearance CX
CX = (UX x V) / PaX
V = urine flow rate (ml/min)
U = urine cons of X (mg/ml)

112
Q

To measure the GFR, what must the substance be ? (HINT: there’s 4 things)

A

Freely filtered at the glomerulus
Neither secreted or reabsorbed
Not metabolised
Not toxic

113
Q

What is the eqn used to calculate GFR?

A

(Uin x V) / Pin

114
Q

Name 6 examples where inflammation is the main pathogenic mechanism?

A 
Filariases
Onchocerciasis
Toxocariasis
Cysticerosis
Schistostomiasis
Enterobius
115
Q

With regards to helminth infections, what causes the inflammation and infection?

A

Wolbachia inside the worm infected

116
Q

What is Diethyl carbamazine? What is its MoA?

A

Piperazine derivative
- inhibits arachidonic acid making parasites more susceptible to immune attack
- good for treatment of filaria infection
- associated with an increase in inflammation
(This is put for completeness)

117
Q

What is the MoA of invermectin? What is it used to treat? What complications/risks can arise?

A

Binds glutamte-gated chloreide increase in the permeability of the cel membrane to chloride ions with hyperpolarisation of the nerve or muscle cell resulting in paralysis and death of the parasite either directly or by causing the worms to starve

  • used against filiarial worms, lice, scabies and bed bugs and is currently being used for the eradication of lymphatic filiariasis and onchocerciasis
  • Complicated by CNS depression and increased risk of absorption past BBB
118
Q

What is the moA of Niclosamide? What is it used for? What is its side effects?

A

Inhibits glucose uptake, oxidative phosphorylation and anaerobic metabolism

  • Used for the treatment of tape worm infections
  • Causes dizziness, skin rashes, drowsiness and perianal itching.
119
Q

What are the 3 methods used to prevent and control intestinal helminths?

A
  1. vector control for filariasis
  2. meat inspection for cysticercosis
  3. sanitation and hygiene for intestinal nematodes
120
Q

Where are ECL cells found? What is its function? How is it stimulated?

A
  • lie deep in the oxyntic glands
  • secretes histamine in response to gastrin
  • it can be stinulated by hormones secreted by the enteric NS
121
Q

Describe acid stimulation by gastrin.

A

Is a polypeptide in 2 forms:
G- 34 and G-17 (more abundant)
- proteins in food have strong effects on gastrin cells, then gastrin is released into blood
- ECL release histamine into oxyntic cells and ECL stimulate HCl release

122
Q

How and when is gastric secretion inhibited?

A

Food in the SI stimulates a reverse enterogastric reflex
Reflex can also be initiated by distension of small bowel, acid in upper intestine, presence of protein breakdown products and irritation of mucosa
(secretin also opposes gastric secretion)

123
Q

Why do oxyntic (parietal) cells have villi like projections?

A

Where HCl is formed by hydrogen potassium pump

124
Q

What makes H. pylori a pathogen for peptic ulcers?

A

Urease produced by the organism raises the gastric pH allowing it to colonise

125
Q

What 3 things is H. pylori infection directly associated with?

A
  1. PEPTIC ULCER DISEASE
  2. GASTRIC CARCINOMA (strone evidence of increased risk)
  3. MALT lymphoma (72-98% infected with h. pylori)
126
Q

Describe an (i) acute infection (ii) chronic infection fo h. pylori.

A

(i) Symptoms = nausea, dyspepsia, malaise and halitosis. Last about 2wks. Gastric mucosa inflamed with neutrophils and inflmmatory cells with marked persistent lymphocyte penetration and stomach acid production falls
(ii) local inflammation and gastritis. The outcome depends on pattern of inflammation, host response, bacterial virulence, environmental factors and pt age

127
Q

What are the consequences of h. pylori infection? (HINT: there’s 8)

A
  1. peptic ulcer disease
  2. distal gastric adenocarcinoma
  3. primary gastric mucosa associated lymphoic tissue lymphome (MALT)
  4. dyspepsia
  5. atrophic gastritis
  6. iron deficiency anaemia
  7. idiopathic thrombocytic purpura
128
Q

What are the 3 ways of managing peptic ulcer disease?

A
  1. Reducing damage to mucosal surfaces (dietary advice, antacids, bismuth)
  2. Killing H. pylori
  3. Reducing gastric acid (proton pump inhibs and H2 blockers)
129
Q

How do we kill h. pylori?

A

Proton pump inhibitor
Ampicillin
- plus either clarithromycin or metronidazole
- if penicillin allergic then use clarithromycin AND metronidazole

130
Q

What is the MoA of histamine blockading drugs? Give 2 examples of this type of drug.

A

They reduce gastric acid by reducing the stimulation of oxyntic cells via the histamine pathway

  • reducing gastric acid, permitting ulcer healing
  • CIMETIDINE = 1st drug to show the value of this approach, RANITIDINE followed and had a better safety profile
131
Q

What is cimetidine?

A

H2 blocker given orally
more than 60% bioavailability and half life = 2hrs
excreted renally

132
Q

What is the adverse event profile of cimetidine?

A

Dizziness

  • cytochrome P450 inhibitor
  • affects hormone metabolism leading to galactorrhea and gynecomastia
  • interferes with tricyclines and serotonin reuptake inhibitors
133
Q

Describe ranitidine. What side effects can it cause?

A

Similar indication to cimetidine

  • now available OTC and well absorbed orally (50%)
  • half life = 2 - 2.5hrs
  • excreted renally
  • malaise and dizziness. liver toxicity and increased risk of GI infection
134
Q

What is the MoA of omeprazole?

A

Inhibits gastric acid secretion by binding irreversible to H+ K+ ATP pump

135
Q

What are the adverse events of omeprazole?

A 
CNS = headaches and dizziness
RESP = upper RTI, cough
GI = abdo pain, diarrhoea, N/V, flatulence, acid regurg and constipation
NM and SKELETAL = back pain, weakness
DERMATOLOGIC = rash
136
Q

What treatment is used for peptic ulcers if you have had a previous exposure and have a penicillin allergy?

A

PPI

  • bismuth
  • metronidazole
  • tetracyclin

(alternative antibiotics include fluoroquinolones)

137
Q

How often does failure of peptic ulcer treatment arise? What treatment is then used?

A

Every 1 in 5

- either an alternative regimen or a quadruple Tx (PPI + bismuth + 2 antibiotics)

138
Q

What is the epidemiology of liver disease in the Scottish population?

A

TIME - the % of liver disease that arises from alcohol has increased in Scotland
PERSON - those over 50 have more chronic liver disease, females more susceptible
PLACE - Scotland high compared to other European countries

139
Q

What are the barriers to reducing alcoholic liver disease in Scotland?

A

ECONOMIC
- alcohol related industries employ approx 155,000 people in Scotland (6% total employment)
- At a UK level alcohol taxes accounts for 7% of all customs and excise revenue
CULTURAL/BEHAVIOURAL
- celebrating end of exams, night out with friends, going on holiday. Alcohol viewed as social lubricant also a perceived social stigma to not drinking
POLITICAL - politicians want to be in office so need to be voted for (economic factors + cultural factors = political barriers)

140
Q

What are the 3 important elements of health promotion?

A
  1. A focus on tackling the determinants of health
  2. Working in partnership with a range of agencies and sectors
  3. Adopting a strategic approach using a range of complementary actions to promote the health of the population
141
Q

What are the roles of the Ottawa Charter for Health Promotion (WHO 1986)? (HINT: there’s 5)

A
  1. developing personal skills
  2. strengthening community action
  3. reorientation health services
  4. building healthy public policy
  5. creating supportive environments
142
Q

What are the 3 components of the Tannahill model of health promotion?

A

Health Education
Prevention
Health protection/Health policy

143
Q

What is the 3 types of health promotion approaches? Describe them.

A
  1. POPULATION approach - aim is to lower the average level of risk factor in the population
  2. HIGH-RISK approach - people particularly at risk are identified through screening , and offered appropriate advice and treatment
  3. TARGETED POPULATION approach - identifying communities at greater risk of disease and using population strategies within these targeted groups
144
Q

When is the population approach useful? Give 2 examples.

A

The disease/risk factor is distributed among large proportions of the population
- the results of not intervening to prevent the disease even if one person are very severe
(adding folic acid to flour, water fluoridation)

145
Q

When is the risk approach useful?

A

It may be difficult to change behaviour at population level

  • when there is concentrated risk within the population
    e. g. bowel cancer screening kits or preventative surgery for women at high risk of breast/ovarian cancer
146
Q

Whose job is it to reduce Alcoholic Liver Disease and Alcohol Related Harm?

A

Bottom line is that it is everyone’s job!!

147
Q

The Scottish government have come up with a framework for changing Scotland’s relationship with alcohol, what are the 4 areas they call for action?

A
  1. reduced alcohol consumption
  2. supporting families and communities
  3. positive attitudes and positive choices
  4. improved treatment and support
148
Q

What 3 ways does the framework for action plan to create supportive environments?

A
  1. Support expansion of diversionary initiatives for young people e.g sports, culture and arts
  2. Promote implementation of workplace alcohol policies
  3. Work with retailers and producers to develop a code of practice for responsible promotion of alcohol
149
Q

What 3 ways does the framework for action plan to build a healthy public policy?

A
  1. Prevent the sale of alcohol as a loss-leader
  2. Introduction of a minimum price per unit of alcohol
  3. 125ml glasses of wine to be the default
150
Q

What 3 ways does the framework for action plan to develop personal skills?

A
  1. Work with partners to improve substance misuse education in schools
  2. Promote awareness and understanding or alcohol misuse and responsible drinking
  3. Support measures to improve alcohol product labelling
151
Q

What 3 ways does the framework for action plan to re-orientate health services?

A
  1. appropriate use of screening tools improves the detection and treatment of alcohol problem
  2. provide a brief national training programme for staff involved in Brief interventions to reduce alcohol consumption
  3. Introduction of new NHS target to deliver brief interventions to reduce alcohol consumption
152
Q

What 2 ways does the framework for action plan to strengthen community action?

A
  1. Support for early intervention such as community initiative to reduce violence
  2. Establishment of a youth commission on alcohol and young people

MD3002 (14 decks)

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