Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical school: 100 cases > 100 Cases in Clinical Pathology > Flashcards

100 Cases in Clinical Pathology Flashcards

1
Q

Whar are the main differentials for sudden-onset polydypsia?

A
  • Diabetes mellitus
  • Diabetes insipidus
  • Hypercalcaemia
  • Primary polydypsia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the causes of non-visible haematuria?

A

Glomerular:

  • Glomerulonephritis
  • Other hereditary causes

Upper urinary tract:

  • Nephrolithiasis
  • Pyelonephritis
  • Renal cell carcinoma
  • Polycystic kidney disease
  • Renal trauma
  • Metabolic derangements such as hypercalciuria

Lower urinary tract:

  • Bladder and prostate cancer
  • Benign lesions such as BPH
  • Bladder papillomas
  • Urethritis
  • Cystitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the investigations for non-visible haematuria in secondary care?

A

Standard for all patients:

  • Urine dip
  • Urine MC&S

Upper urinary tract-specific:

  • Ultrasound/CT systography

Lower urinary tract-specifc:

  • Cystoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of hypertonic hyponatraemia?

A

Presence of osmotic agents in the blood drawing water out of cells. This occurs with hyperglycaemia and infusion of osmotic agents like mannitol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the causes of isotonic hyponatraemia?

A
  • Retention of isosmotic fluid in the extracellular space (e.g. isotonic glucose infusion)
  • Severe hyperlipidaemia or hyperproteinaemia reduces the fractional water content, leading to a ‘pseudohyponatraemia’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of hypotonic hyponatraemia?

A

Hypovolaemic:

  • Sodium depletion by renal or extrarenal means

Normovolaemic:

  • Sodium content is diluted by excess amounts of water
  • SIADH
  • Hypothyroidism
  • Reduced solutes intake

Hypervolaemic:

  • Retention of sodium and water due to activation of the renin-angiotensin-aldosterone system
  • Congestive heart failure
  • Liver cirrhosis
  • Nephrotic syndrome
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the criteria for diagnosing SIADH?

A
  1. Reduced plasma osmolality <275 mOsm
  2. Urine osmolality >100 mOsm
  3. Clinical euvolaemia
  4. Continued natriuresis >40 mM in the presence of…
  5. Normal thyroid and adrenal function, and
  6. Without recent use of diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of nephrotic syndrome?

A

Primary glomerular disease:

  1. Minimal change disease
  2. Membranous glomerulopathy
  3. Focal segmental glomerulosclerosis (FSGS)
  4. Membranoproliferative glomerulonephritis (MPGN)

Systemic diseases:

  1. Diabetes mellitus
  2. Amyloidosis
  3. Systemic lupus erythematosus
  4. Drugs (e.g. nonsteroidal anti-inflammatories [NSAIDs])
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What conditions are associated with +ve ANA?

A
  • Systemic lupus erythematosus (SLE)
  • Scleroderma
  • Rheumatoid arthritis
  • Mixed connective tissue disease
  • Sjögren’s syndrome
  • Inflammatory myopathies, such as dermatomyositis and polymyositis
  • Primary biliary cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the criteria for a good screening test?

A
  • The disease being screened should be an important health problem
  • The natural history of the disease should be well understood
  • There should be an identifiable early stage of disease
  • Treatment at an early stage should be of more benefit than at a later stage
  • There should be a suitable test to identify the early stage
  • The test should be acceptable to the population
  • The intervals for repeating the test should be well defined
  • Suitable facilities should exist to account for the workload resulting from screening
  • Risks of the test, both physical and psychological, should be less than the anticipated benefits
  • Costs should be balanced against benefits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of hypoglycaemia?

A

Non-fasting (occurs after meal):

  • Gastrectomy/bypass surgery (which causes rapid gastric emptying with overproduction of insulin)
  • Pancreatic islet cell hyperplasia
  • Occult diabetes (deficient early insulin response in diabetes followed by exaggerated delayed response)

Fasting (between meals):

Hyperinsulinaemic state

  • Insulin reaction or sulphonylurea overdose (the commonest cause)
  • Autoimmune hypoglycaemia
  • Surreptitious use of insulin or sulphonylureas
  • Pancreatic β-cell tumours (typically insulinoma)

Non-hyperinsulinaemic state:

  • Reduced hepatic gluconeogenesis, which may arise from liver disease or inborn
    errors of metabolism
  • Renal insufficiency (the kidney contributes to gluconeogenesis too)
  • Alcohol excess, which increases the activity of alcohol dehydrogenase (consuming
    NAD+) and thereby limits the conversion of lactate to pyruvate, which is a
    gluconeogenic substrate
  • Non-pancreatic tumours (e.g. retroperitoneal fibrosarcoma) that release IGF-2,
    which can activate the insulin receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the metabolism of bilirubin?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What levels of serum bilirubin are required to produce jaundice?

A

>50 uM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the mechanisms of hyperbilirubinaemia?

A
  1. Excess production
  2. Reduced hepatic uptake
  3. Impaired conjugation
  4. Reduced hepatocellular excretion
  5. Impaired bile flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the types of jaundice?

A
  • Pre-hepatic. This causes an unconjugated hyperbilirubinaemia and arises from increased production of bilirubin (e.g. haemolysis, ineffective erythropoiesis).
  • Hepatic. The hyperbilirubinaemia may either be conjugated or unconjugated depending on which part of the hepatic metabolic pathway is affected. Congenital causes include Gilbert, Crigler–Najjar, and Dubin–Johnson syndromes, while acquired causes include viral hepatitis, autoimmune hepatitis, alcoholic liver disease, drugs (e.g. halothane, paracetamol and methyldopa) and primary biliary cirrhosis.
  • Post-hepatic. This typically causes a conjugated hyperbilirubinaemia and arises as a result of biliary obstruction, causes of which include gallstones, malignancy (pancreatic cancer, cholangiocarcinoma and ampullary tumours of the duodenum), biliary strictures, pancreatic pseudocysts, and sclerosing cholangitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of hypercalcaemia?

A
  • Hyperparathyroidism, which may be primary (e.g. parathyroid adenoma), secondary
    (from renal failure leading to hyperphosphataemia and stimulation of parathyroid hormone [PTH] secretion), or tertiary (autonomous parathyroid activity
    arising from secondary hyperparathyroidism)
  • Malignancy-associated, which may be either humorally mediated (e.g. release of PTHrP from squamous cell carcinomas) or osteolytic (e.g. multiple myeloma and bone metastases)
  • Vitamin D-related (granulomatous diseases such as sarcoidosis, vitamin D excess)
  • Drug-induced (e.g. thiazide diuretics)
  • Endocrine disorders, including thyrotoxicosis
  • Genetic disorders (e.g. familial hypocalciuric hypercalcaemia, FHH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the most common causes of hypercalcaemia?

A
  • Hyperparathyroidism
  • Malignancy
  • Together, these account for 90% of cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How should hypercalcaemia be investigated?

A
  1. Investigate serum PTH
  2. If high, suspect primary or tertiary hyperparathyroidism
  3. If low, probably due to feedback suppression, suspect malignancy
  4. If inconclusive, look at serum vitamin D and serum ACE (sarcoidosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is hirsutism?

A

Excessive terminal hair growth in a male pattern in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a Ferriman–Gallwey scale?

A
  • Scoring system used to determine amout of hair growth in androgen-dependent areas of the body
  • A score of >7 is considered hirsutism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the causes of hirsutism in women?

A

Non-pathological:

  • Idiopathic hirsutism (around 50% of cases)

Pathological:

  • Polycystic ovarian syndrome
  • Adrenogenital syndromes (e.g. nonclassic congenital adrenal hyperplasia)
  • Androgen-secreting tumours,
  • Causes of hormone over-production such as Cushing’s syndrome
  • Drug-induced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are important secondary causes of immunosuppression?

A
  • Infections (e.g. HIV)
  • Malnutrition
  • Malignancy (especiially haematological)
  • Drugs (e.g. immunosuppressants)
  • Protein loss (e.g. nephrotic syndrome, protein-losing enteropathies)
  • Metabolic diseases (e.g. diabetes, severe liver disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the common causes of primary immunodeficiency?

A
  • Common variable immunodeficiency
  • X-linked agammaglobulinaemia
  • Selective Ig subclass deficiency
  • Hyper-IgM syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the normal range for anion gap?

A

10 - 18 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the common causes of metabolic acidosis with normal anion gap?

A

Metabolic acidosis with normal anion gap is caused by excess retention of H+ or loss of HCO3. Causes include:

  • Increased losses of HCO3 from the gut (e.g. diarrhoea, via stomas)
  • Increased losses of HCO3 from the kidney (e.g. carbonic anhydrase inhibitor therapy, proximal or type 2 renal tubular acidosis, tubular damage from drugs or paraproteins)
  • Reduced renal excretion of H+ (e.g. distal or type 1 renal tubular acidosis, and type 4 renal tubular acidosis)
  • Increased production of HCl (e.g. ingestion of ammonium chloride)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the pre-renal causes of AKI?

A

Arises from hypovolaemia leading to inadequate renal blood flow:

  • Haemorrhage
  • Sepsis
  • Heart failure
  • Diarrhoea
  • Use of diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the renal causes of AKI?

A

Intrinsic renal disease, which may affect the glomeruli:

  • Glomerulonephritides

Intrinsic renal disease, which may affect the tubules and interstitium:

  • Drugs such as NSAIDs and aminoglycosides
  • Contrast media
  • Intra-renal obstruction arising from renal calculi or the

cast nephropathy in multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the post-renal causes of AKI?

A

Post-renal obstruction, which leads to renal failure when both outflow tracts are obstructed or when one is obstructed in patients with a single kidney:

  • Bladder outflow obstruction
  • Ureteric calculi
  • Intratubular crystal nephropathy
  • Urothelial neoplasms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the causes of ambiguous genitalia in virilised females?

A
  • Androgens of fetal origin (e.g. congenital adrenal hyperplasia [CAH])
  • Androgens of maternal origin (e.g. drugs such as progesterone and danazol, maternal androgen-secreting tumours of the ovary or adrenal gland) origin
  • Dysmorphic conditions such as Beckwith–Wiedemann and Seckel syndromes
30
Q

What are the causes of ambiguous genitalia in unvirilised males?

A
  • Biosynthetic defect leading to reduced fetal androgen production (e.g. Leydig cell defects, 5-α-reductase deficiency deficiency, anti-Müllerian hormone)
  • End-organ unresponsiveness to androgens (androgen insensitivity syndrome), dysmorphic syndromes (e.g. Smith–Lemli–Opitz syndrome)
  • Testicular dysgenesis or malfunction
31
Q

What is the process of examining a child with ambiguous genitalia?

A
  1. Take detailed history looking for any use of drugs that can cause female virilisation
  2. Examine the mother and look for evidence of female virilisation (suggestive of androgen-secreting tumour)
  3. Ask about family history of genetic conditions that lead to ambiguous genitalia
  4. Fully examine the child and look for dysmorphic features sugestive of underlying disease
  5. Examine the external genitalia and look for:
  • Number of gonads
  • Degree of virilization
  • Length of the phallus
  • Any hyperpigmentation that would suggest excessive adrenocorticotropic hormone (ACTH) production
  1. Karyotyping
  2. Use ultrasound to determine internal pelvic anatomy
  3. Blood tests including U&Es (avoid salt crisis due to CAH), LH, FSH and androgens (testosterone, DHEA, androstenedione and 17-OH-progestrone)
32
Q

What are the common ACTH-dependent causes of Cushing’s syndrome?

A
  • ACTH-producing pituitary adenoma (Cushing’s disease)
  • Ectopic production of ACTH from other tissues (e.g. part of paraneoplastic phenomenon of small cell lung cancer)
33
Q

What are the common ACTH-independent causes of Cushing’s syndrome?

A
  • Exogenous corticosteroid use
  • Cortisol-producing adrenal neoplasm
  • Adrenal hyperplasia
34
Q

When should secondary hypertension be considered in an individual?

A
  • Young patients
  • Those with very high blood pressure (>180/110 mmHg)
  • Absence
    of risk factors for essential hypertension
  • History of hypertensive emergencies
  • Severe or progressive target organ damage (e.g. deteriorating renal function)
  • Particular symptoms or signs suggestive of an underlying cause (e.g. palpitations, flushing)
35
Q

What are the causes of secondary hypertension?

A
  • Renal, including renal parenchymal disease, renal artery stenosis and renin-producing tumours
  • Endocrine, including primary aldosteronism, Cushing’s syndrome, phaeochromocytoma, acromegaly, and hypo- or hyperthyroidism
  • Cardiac (coarctation of the aorta)
  • Neurologic, particularly raised intracranial pressure and stress
  • Other, including obstructive sleep apnoea and drugs (e.g. steroids, NSAIDs)
36
Q

What are the main groups of causes for hypokalaemia?

A
  1. Reduced intake of K
  2. Transcellular movement of K
  3. Increased excretion of K
37
Q

What are the common causes of transcellular movement of K leading to hypokalaemia?

A
  • Alkalosis (since K and H tend to move in opposite directions. As H moves out of cells to compensate for alkalosis, K moves into cells)
  • Insulin
  • Use of beta-agonists
  • Refeeding syndrome
38
Q

What are the common causes of increased K excretion leading to hypokalaemia?

A

Renal:

  • Diuretics
  • Diuretic phase of acute renal failure
  • Mineralocorticoid excess

Extra-renal:

  • Diarrhoea
  • Vomiting
  • Excess sweating
  • Villous adenomas of the rectum
39
Q

What is the physiological consequence of hypokalaemia?

A

The direct physiological consequene of hypokalaemia is the hyperpolarisation of membranes leading to difficulty in the firing of action potentials

40
Q

What are the effects of hypokalemia on organ systems?

A
  • Heart defects
  • Constipation
  • Ileus
  • Rhabdomyolysis
  • Respiratory muscle weakness resulting in ventilatory failure
  • Impaired ability to concentrate urine leading to nephrogenic diabetes insipidus
    *
41
Q

What are the ECG changes asssociated with hypokalaemia?

A
  • Increased amplitude and width of the P wave
  • Prolongation of the PR interval
  • T wave flattening and inversion
  • ST depression
  • Prominent U waves (best seen in the precordial leads)
42
Q

What is the physiological mechanism behind primary hypogonadism in men?

A
  • Primary hypogonadism is caused by a testicular dysfunction leading to reduced production of testosterone
  • This subsequently causes lack of -ve feedback in production of gonadotrophins (LH & FSH), leading to the term hypergonadotrophic hypogonadism
43
Q

What are the causes of primary hypogonadism in men?

A

Congenital:

  • Klinefelter’s syndrome
  • Testicular agenesis
  • Enzyme defects such as 5-α-reductase deficiency

Acquired:

  • Mumps orchitis
  • Bilateral testicular injury or torsion
  • Irradiation to the testes, and effects of cytotoxic drugs
44
Q

What are the causes of secondary hypogonadism in men?

A
  • Pituitary dysfunction (tumours or hypopituitarism)
  • Hypothalamic disorders (e.g. Kallman’s syndrome)
  • Obesity
  • Drugs
45
Q

What are the causes of primary hypercholesterolaemia?

A

Genetic (familial hyperchoesterolaemia)

46
Q

What are the causes of secondary hypercholesterolaemia?

A
  • Hypothyroidism
  • Diabetes mellitus
  • Obesity
  • Nephrotic syndrome
  • Renal and liver failure
  • Drugs (e.g. thiazides, antiretrovirals)
  • Alcohol
47
Q

What are the dangers a patient may face imediately following bone marrow transplantation?

A
  • Infection (due to low WBC count or immunosuppression)
  • Bleeding (due to low platelet counts)
  • Graft vs host disease
48
Q

What are considered fragility fractures?

A
  • Colles’ fracture (of forearm)
  • Fractured neck of femur
  • Vertebral body fracture
49
Q

What are the mechanisms of rejection following organ transplantation?

A
  • Hyperacute rejection
  • Acute rejection
  • Chronic rejection
50
Q

What are the mechanisms of hyperacute rejection?

A
  • Occurs within minutes of the graft perfusion in the operating theatre
  • It is characterized by a type II antibody-mediated hypersensitivity reaction whereby pre-existing anti-graft antibodies in the recipient bind to foreign antigens. This results in opsonization with phagocytes engulfing cells that have been marked by antibodies.
  • The antibodies activate complement, which enhances phagocytosis, and causes cell lysis.
  • The treatment for hyperacute rejection is immediate removal of the graft
51
Q

What are the mechanisms of acute rejection?

A
  • Takes place a number of weeks after the transplant
  • It is characterized by cell-mediated toxicity by cytotoxic T-cells. This process involves host CD4 T-cells recognising foreign antigens (on the graft) and producing cytokines such as IL-2 that stimulate cytotoxic T-cells, which are able to initiate apoptosis of the foreign tissue.
  • The treatment for acute rejection includes high dose steroids.
52
Q

What are the mechanisms of chronic rejection?

A
  • Takes place months to years after the transplant.
  • It is irreversible and characterized by both cell-mediated (cytotoxic T-cell) and antibody mediated (humoral) immune reactions that result in fibrosis and obliteration of the blood vessels of the transplanted organ.
  • As it is irreversible, treatment for chronic rejection is difficult, and may include re-transplantation.
53
Q

What regime of immunosuppressants are transplant recipients generally placed on?

A

Triple therapy consisting of:

  • Corticosteroids
  • Azathioprine
  • Ciclosporin/tacrolimus
54
Q

What are the features of acute rejection of liver transplant?

A
  • Generally speaking, rejection of liver begins in biliary epithelium rather than vascular endothelium
  • Features of include elevated bilirubin and deranged LFT
55
Q

What features in family history would suggest a hereditary breast cancer syndrome?

A
  • Early-onset breast cancer (<50 yrs)
  • Bilateral cancers
  • Particular ethnicity (e.g. Ashkenazi Jews)
  • Any male breast cancer
  • Other associated cancers (e.g. ovarian, peritoneal or fallopian tube)
56
Q

What are the common causes of hypocalcaemia?

A
  • Hypoalbuminaemia (most common as 40% of Ca in serum bound to albumin; either due to reduced synthesis due to liver failure or excess loss from nephrotic syndrome)
  • Autoimmune or congenital hypoparathyroidism
  • Vitamin D deficiency
  • Loop diuretics
57
Q

Which structures are at risk of aneurysm formation?

A
  • Abdominal aorta
  • Other arteries in the peripheral circulation (iliac, femoral and popliteal arteries) - Rare
  • Thoracic aorta - Expecially associated with late stage syphilis and inherited connective tissue disorders such as Marfan’s
  • Coronary arteries - Usually secondary to Kawasaki disease
  • Cardiac walls - Secondary to MI
  • Cerebral circulation - Berry aneurysms
58
Q

What is a false aneurysm?

A
  • Contained collections of blood immediately
    outside a vessel, but where there is still a direct communication through a defect in the vessel wall
  • This usually occurs following trauma, commonly iatrogenic trauma caused during arterial puncture required for percutaneous transarterial interventional procedures
59
Q

What are the indications for a tracheostomy in children?

A
60
Q

What are the differences between true and apparent polycythaemia?

A
  • True polycythaemia is when there is an actual increase in total red cell mass while apparent polycythaemia is when there is seemingly raised haematocrit and PCV secondary to reduced plasma volume
61
Q

What are the causes of primary polycythaemia?

A
  • Polycythaemia vera
  • Inherited defect in EPO receptor
  • Inherited defect in RBC precursors
62
Q

What are the causes of secondary polycythaemia?

A

Hypoxia-dependent:

  • Severe lung disease
  • Heavy smoking
  • Cyanotic heart disease

Hypoxia-independent:

  • Elevated EPO secondary to inherited disorder, renal disease or liver disease
  • Endocrine disorders such as Cushing’s or Conn’s syndrome
63
Q

How is acute leukaemia distinguished from chronic leukaemia?

A
  • On blood film, chronic leukaemia is characterised by clonal expansion of affected WBCs at all stages in development while in acute leukaemia, only blast cells are expanded
  • Chronic leukaemia is generally not associated with bone marrow failure while acute leukaemias are
64
Q

What important questions need to be considered when presented with a patient that bruises easily?

A
  • Whether this level of bruising is normal for a patient
  • Whether the patient has had any bleeding (e.g. epistaxis, haematuria,
    menorrhagia, haemoptysis) and have a high level of suspicion for intracranial haemorrhage
  • Whether there’s been any previous surgical (including dental) interventions that have led to bleeding problems
65
Q

What are the threshold platelet counts for certain procedures?

A

> 100 x 109/L - Neurosurgical, ophthalmological operations

>80 x 109/L - Epidural, lumbar puncture

>50 x 109/L - All other surgical procedures

66
Q

What are the common causes of retroperitoneal tumours?

A
  • Lymph node metastases from organs draining into para-aortic lymph nodes (including much of the lower GI tract)
  • Germ cell tumours
  • Lymphoma (Hodgkin’s and non-Hodgkin’s)
67
Q

What are the common causes of acute red eyes?

A
  • Acute conjunctivitis
  • Anterior uveitis (inflammation of the anterior structures of the uvea [the pigmented vascular inner layer of the eye comprising the iris, ciliary body and
    choroid])
  • Corneal ulcers
  • Acute closed-angle glaucoma
  • Trauma with subconjunctival haemorrhage
  • Allergic conjunctivitis
  • Measles
  • Episcleritis
68
Q

What are the common causes of maculopaular rashes (no vesicles) in children?

A
  • Measles: Prodrome – Coryza, cough, conjunctivitis. Rash on
    face, neck and shoulders. Koplik’s spots on mucous
    membranes. Vaccine-preventable.
  • Scarlet fever: Sore throat, generalized rash with perioral sparing,
    strawberry tongue, skin peeling following rash.
  • Rubella: Rapidly fading lacy rash begins on face and spreads to
    trunk and limbs. Suboccipital lymphadenopathy.
    Vaccine preventable.
  • Fourth disease
  • Erythema infectosum (fifth disease): Slapped cheek rash, lacy rash, anaemia.
  • Roseola infantum (sixth disease): Pink rash beginning on trunk and spreading out to face, neck and limbs. Sore throat and red eyes.
  • Kawasaki disease
69
Q

What are the most common causes of fever in a returning traveller?

A
  • Malaria
  • Typhoid fever
  • Hepatitis
  • Dengue
  • Yellow fever
  • Schistosomiasis
  • Meningitis
  • HIV
70
Q

What tests should be carried out in person presenting with fever with recent travel history?

A
  • Full blood count and clotting screen, as bleeding can occur in the haemorrhagic fevers (Dengue and yellow fever), meningococcal sepsis, malaria (owing to low platelets) and hepatitis (if severe liver dysfunction occurs).
  • Liver function tests, as jaundice may occur in malaria, typhoid, hepatitis, dengue, yellow fever, schistosomiasis and meningococcal disease if there is severe sepsis.
  • Blood cultures to exclude typhoid (abdominal pain, endemic area, fever, low platelets, low white blood cells), and meningococcal disease (endemic area, fever, low platelets).
  • Malaria film
71
Q

What are the classicla congenital infections?

A

TORCHES

Toxoplasma

Other (VZV, parvovirus B19, coxackievirus, HIV)

Rubella

CMV

HErpes simplex

Syphilis

72
Q

What are the causes of urethral discharge?

A
  • Gonococcal urethritis (Neisseria gonorrhoea)
  • Non-gonococcal urethritis:
  1. Chlamydia trachomatis
  2. Mycoplasma genitalium
  3. Trichomonas vaginalis
  4. Ureaplasma urealyticum
  5. Herpes simplex virus
  6. Prostatitis

Clinical school: 100 cases (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions