Paper 2 Flashcards

(47 cards)

1
Q

The islets of Langerhans are complex mini organs which are essential for maintaining glucose homeostasis. Briefly outline the important structural components of pancreatic islets, and include in your answer the hormones secreted by each cell type, and their functions.

A

To include: Insuloacinar portal system, capillary plexus & anastomosing cords of cells, branches of sympathetic and parasympathetic nerves (vagal), interneurons Beta cells – Insulin – cellular uptake of glucose (Glut4) – endocrine Alpha cells - Glucagon –- > hepatic glycogenolysis – endocrine
Delta cells - Somatostatin & gastrin –– SS inhibits glucagon & insulin release (paracrine – intraislet signalling)
F / PP cells - Pancreatic polypeptide –– inhibits somatostatin secretion– paracrine (also inhibits secretion of pancreatic enzymes and bile from gall bladder - endocrine) (also inhibits secretion of pancreatic enzymes
and bile from gall bladder - endocrine)

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2
Q

State which cell types provide myelination in the central nervous system (CNS) and peripheral nervous system (PNS), respectively.

A

Oligodendrocytes and Schwann cells

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3
Q

Briefly describe the main structural differences between the above cell types and their relationships to the axons.

A

Oligodendrocytes – one cell can myelinate several axon segments; Schwann cells – each cell myelinates only one axon segment
Both speed impulse transmission throughout the axon.

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4
Q

Explain how the myelin-forming cells of the PNS support axon regeneration.

A

Removal/recycling of cell debris;
provision of axon-growth promoting substrate (cell adhesion molecules); promotion of survival of injured neurons (neurotrophic factor release)

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5
Q

If Mr. Hanlie suffered damage to his brain tissue, briefly explain how survival of the neurons could be affected.

A

Immediate cell death (necrotic), as well as delayed death (apoptotic) through inflammatory processes, metabolic and respiratory stress

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6
Q

State whether disrupted connections between neurons in the injured brain are likely to functionally restore themselves. Provide the reasons for your
answer.

A

No, as injured CNS neurons often degenerate or fail to re-express the genes necessary for axonal regeneration. The CNS microenvironment (glia: oligodendrocytes, astrocytes and microglia) is not conducive for axon regrowth, and molecular guidance cues are not re-expressed in the adult brain

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7
Q

State under what name are the histological features of degenerating axonal pathways known.

A

Wallerian degeneration

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8
Q

Name the cutaneous mechanoreceptor that detects high-frequency vibration. (1⁄2 mark). State whether this receptor is rapidly or slowly adapting.

A

Pacinian corpuscle. Rapidly-adapting.

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9
Q

Give a concise definition of “sensory transduction” as applied to the somatosensory system

A

conversion of the physical (or chemical) energy stimulus into an electrical signal in a sensory neuron

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10
Q

List and discuss a three-step sequence of events to explain how vibration sense on the skin is converted into neuronal activity.

A

Step 1: Mechanical stimulus (e.g. pressure) deforms the receptor’s (Pacinian corpuscle) onion-like outer membrane.
Step 2: The receptor’s channels open and Na+ flows through membrane. The inside of the receptor
(1 marks)
depolarizes (voltage becomes more positive).
Step 3: If the graded potential (summed at the initial segment) is above a threshold level, action potentials are generated and propagated down the axon. Cutaneous mechanoreceptor afferents have myelinated axons in which action potentials jump from gap to gap in the myelin sheath. This sheath insulates the axon and speeds up the conduction of action potentials.

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11
Q

The response to a somatosensory stimulus has the ability to adapt. Explain how this occurs by using the Pacinian corpuscle as an example of a cutaneous mechanoreceptor.

A

The number of action potentials/second adapts because the receptor potential adapts. The receptor potential adapts in part because the onion-like laminae in Pacinian corpuscle. corpuscle slip back to their original shape, closing the channels.

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12
Q

Outline three (3) factors that predispose a patient to the pathogenesis of a diabetic foot.

A

Sensory neuropathy resulting in traumatic injury- accumulation of sorbitol and fructose in the schwaan cells.
b. Macrovascular – accelerated atherosclerosis- occlusion of vaso nervosa
c. Hyperglycemia predisposes to infection- poor inflammatory response to bacteria.

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13
Q

List four (4) complications of uncontrolled diabetes involving the kidney.

A

Nodular glomerulosclerosis (Kimmelstiel- Wilson)
- Diffuse glomerular basement membrane thickening with proteinuria - Pyelonephritis
- Renal papillary necrosis

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14
Q

List four (4) causes for a falsely increased level of HbA1c.

A

Iron deficiency anaemia
Splenectomy
Aplastic anaemia
Haemoglobinopathies (depends on method)

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15
Q

Name the biochemical class of hormone to which insulin belongs.

A

Peptide/ protein

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16
Q

Outline what happens to extracellular phosphate when insulin is administered.

A

When insulin is administered, glucose leaves blood and enters the cells via Glut-4. Phosphate It moves intracellularly and EC levels can decrease for glucose phosphorylation, an thus K + and Mg^2+ follows to maintain electroneutrality (intracellular levels drops)

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17
Q

Name (in full) the most likely organism responsible for this infection.

A

Clostridium perfringens

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18
Q

Briefly describe the pathogenesis of this infection.

A

Poor blood supply to the area thus less oxygen and anaerobes proliferate (1) also exotoxins produced by
organism (1

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19
Q

State the laboratory conditions that this organism requires in order to be cultured.

A

Anaerobic conditions

20
Q

Briefly describe how you would manage this case.

A

Treat underlying cause/diabetes (1) Remove necrotic tissue (1) Penicillin or metronidazole (1)

21
Q

The doctor decided to perform a thorough examination and finds that Miss Alberts has red itchy patches in her groin area. He suspects a yeast infection.
82. Name (in full) the organism that is the most likely causing the infection.

A

Candida albicans

22
Q

Briefly describe how you would manage this condition candida.

A

Topical antifungal like nystatin/clotrimazole (amphotericin B / fluconazole (1/2) and correct underlying
condition (1/2), keep area dry (1/2)

23
Q

Outline one reason why this infection is present in this patient.

A

The patient is diabetic which is an immunocompromised state

24
Q

Outline why this infection is particularly common at this site.

A

The groin is a moist and warm fold area thus ideal for growth of yeast

25
. Describe the arterial supply to the choroid plexus in ventricles 1-3 and in ventricle 4.
Anterior choroidal arteries arise from anterior circulation = middle cerebral artery, pass through brain tissue and invaginate into the ventricles via choroid fissure, ventricles 1-3. Posterior choroidal arteries arise from various places in the posterior circulation and invaginate into the roof of ventricle 4 (inferior medullary velum) – also via choroid fissure.
26
Briefly describe the structures providing physiological barriers that protect the brain.
Cerebral capillaries (non-fenestrated endothelium with tight junctions and selective transport mechanisms, thick basement membrane, astrocyte foot processes); choroid plexus (CSF-secreting villi covered by choroid epithelium with barrier function); meninges (arachnoid and pia with barrier and arachnoid trabecular cells)
27
State where the ependymal cell layer is found.
Inner lining of the ventricles and central canal
28
State whether the ependymal cell layer is a true physiological barrier. Provide its structural features in support of your answer.
No, lack of a solid basement membrane and few tight junctions
29
Describe the typical CSF cell count and chemistry findings in bacterial meningitis.
Polymorphs- increased Lymphocytes- <6 or none Red blood cells- 0 Glucose- decreased Protein- increased
30
Name (in full) two (2) organisms that commonly cause acute bacterial meningitis.
Streptococcus pneumoniae and Neisseria meningitidis
31
Outline ante-mortem and post-mortem testing of a person with suspected rabies.
Ante-mortem – CSF, saliva, blood (for antibodies if not previously vaccinated), (corneal smears, nuchal biopsy) Post-mortem – brain tissue in formalin for histology and glycerol-saline or saline for virology
32
Define the following terms: meningitis, myelitis, encephalitis, meningoencephalitis encephalomyelitis
Meningitis – inflammation of the meninges Myelitis – inflammation of the spinal cord Encephalitis – inflammation of the brain parenchyma Meningoencephalitis – inflammation of both meninges and brain parenchyma Encephalomyelitis – inflammation of both brain parenchyma and spinal cord
33
Compare and contrast herpes simplex meningitis and herpes simplex encephalitis.
Meningitis – usually with genital infection / reactivation; mild condition; good prognosis; no treatment needed. Encephalitis – mostly with HSV-1 reactivation, sometimes neonatal HSV; severe condition; high mortality without treatment, high morbidity; urgent acyclovir prior to obtaining lab results.
34
State the hallmark finding on CSF protein electrophoresis that suggests a diagnosis of multiple sclerosis.
Oligoclonal bands CSF findings: Proteins increased, WCC increased, IgG index increased, CSF myelin basic protein increased
35
Name the two (2) biochemical analytes that are responsible for most cases of cerebrospinal fluid xanthochromia.
Bilirubin Protein
36
Froin’s Syndrome (Xanthochromia, Protein above (1.5 g/L) and viscous CFS that clots due to activation of exudative clotting. 97. State what the CSF IgG index is used for.
To differentiate/ screen for intrathecal production of immunoglobulins in cases of high CSF protein. Normal index <0.7, increased permeability- high index of 1 - Multiple sclerosis - Chronic inflammation in CNS - Neurological diseases where B lymphocytes are induced to migrate from the blood into the brain- clonal expansion and differentiation into plasma cells- Ig production intrathecally Other CSG protein markers - Albumin, - ADA (adenosine deaminase- may be elevated in TB meningitis) - LDH4 and LDH5 isoenzymes increased with CNS tumours - HCG may be increased with metastatic choriocarcinoma.
37
Briefly explain why CSF glucose does not increase beyond approximately 10mmol/L in cases of severe hyperglycaemia (uncontrolled diabetes).
Glucose transporters become saturated and cannot transport more glucose into CSF
38
Outline the determinants and distribution of meningococcal disease in South Africa.
Determinants Neisseria Meningitidis causative organism (0.5) Spread by droplets spread person to person or intimate contact with nasopharyngeal secretions (1) Some people are carriers of the organism (5-10%) (0.5), Colonisation with N. meningitidis usually confers protection through the production of antibodies to that particular strain. Infrequently, newly acquired hypervirulent carriage strains are able to invade the mucosa and cause bacteraemia and/or Meningitis (1). (1.5) Risk factors: Some people are carriers of the organism (5-10%), Carriage increased in: smokers (0.5) and passive smokers (0.5), overcrowded households (0.5), new military recruits (0.5), and first year resident students at universities/Technicons (0.5), intimate personal contact (kissing), pub attendance, mass gatherings (0.5), previous antibiotic use(0.5) Other risk factors: Co-existing viral infection (0.5) HIV (0.5), other immune deficiencies esp. of the complement component system (0.5), asplenia (0.5) Household contacts have much higher (400-800) old increase risk of infection (0.5) Household overcrowding (0.5) Distribution In SA: Seasonal increase in winter & early spring (may-oct) (1). During these times outbreaks may occur especially in mines, correctional & detention facilities, academic institutions, displaced communities (1) N. Meningitis has 12 serogroups. Serogroup W & B causes majority of disease in South Africa (1) - other immunocompromising conditions
39
Explain the difference between primary and secondary neurulation in an embryo.
There are two major ways of forming a neural tube. In primary neurulation, the cells surrounding the neural plate direct the neural plate cells to proliferate, invaginate, and pinch off from the surface to form a hollow tube. In secondary neurulation, the neural tube arises from a solid cord of cells that sinks into the embryo and subsequently hollows out (cavitates) to form a hollow tube. The medullary cord may be formed by ectoderm, mesoderm or even endoderm, according to the species. The extent to which these modes of construction are used varies among vertebrate classes.
40
Define the term macrosomia and explain why this may occur during uncontrolled gestational diabetes and how the neonate will present.
Large gestational age (LGA) or macrosomia is a term used to describe a neonate with an excessive birth weight due to a range of causes. There are many different definitions that have been used for to this term, generally a birth weight of 4 to 4.5kg. In the context of our PBL cases, gestational diabetes or DM type 2 with poorly controlled blood glucose levels in the mother. Glucose crosses placenta = considerable growth occurs. Caesarian section, jittery baby due to hypoglycaemia, risk for DM Type 2 later in life.
41
During pregnancy a biochemical prenatal screening test can be performed for neural tube defect. 102. State at what stage of pregnancy this screening test is performed.
15 to 20 weeks’ gestation. (Can give a mark for 16 to 18 weeks’ gestation. Can give 1⁄2 mark for “in the second trimester”.)
42
Name the biochemical marker that is measured in the mother’s blood to determine the risk of the fetus having an open neural tube defect.
Alpha-fetoprotein
43
The result of this biochemical test is typically reported both as a concentration, as well as in a second unit normalized for maternal age and gestational age. State this second unit. List both its short form and its full name.
MoM Multiple of the Median
44
Define six (6) characteristics of a good screening test.
Any 4 of these: Reasonable cost Easy to perform Safe and preferably non-invasive Reproducible results Must be able to detect disease or condition at a time when it can still be managed Low false negative rate
45
Briefly explain why you think the baby has club feet.
The nerve supply to the lower limbs will be disrupted due to the lumbar NTD reducing leg and foot mobility. It may also be a sign of a syndromic NTD.
46
Sindy’s boyfriend tells her his sister has spina bifida and his father had a baby brother whose brain didn’t develop and died when he was 2 hours old. State what kind of inheritance you would suspect in this family.
Multi factorial inheritance
47
Sindy has broken up with her boyfriend and asks if she should do anything different in her next pregnancy. Describe what you would advise her.
Plan the pregnancy Ensure optimal nutrition at conception and through pregnancy with balanced diet Avoid teratogens – alcohol, drugs if could become pregnant (not only when pregnancy established) If taking medication discuss with doctor before pregnancy if the safest option High dose periconceptual folic acid – 4/ 5 mg folic at least 1 month before and 3 months after conception Screening for NTD in next pregnancy – ultrasound +/- maternal serum AFP