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MBBS VI - SpC - Family Medicine > Constitutional problem - Fever > Flashcards

Constitutional problem - Fever Flashcards

1
Q

Define normal oral, rectal, tympanic and axillary temp

A

Oral: 33.2-38.2
Rectal: 34.4-37.8
Tympanic: 34.4-37.8
Axillary: 35.5-37.0

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2
Q

Determinants of basal body temperature

A

Age, sex, time of measurement (diurnal pattern and ovulation pattern), activity level, illnesses

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3
Q

Describe the physiological responses to increase body temperature

A

Increase temperature detected by temperature-sensitive receptors in skin and hypothalamus

Increase voluntary responses:

  • Reduce activity
  • Loose clothing
  • Expose body to cold environment
  • Cooking drink

Hypothalamus activates cooling mechanisms:

  • Increase parasympathetic nervous system - Increase sweating
  • Decrease sympathetic nervous system - increase vasodilation and decrease basal metabolic rate
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4
Q

Describe physiological responses to hypothermia

A

Voluntary responses:

  • Eat
  • Seek heat source
  • Increase muscle activity
  • Warm clothing

Hypothalamic response:

  • Increase thyroid hormone - increase BMR
  • Increase sympathetic nervous system: Vasoconstriction, Increase BMR, Piloerection
  • Increase shivering
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5
Q

Physiological mechanism of pyrexia at the hypothalamus

A

1 .Infections releases LPS and causes Monocyte activation/ LPS directly enters hypothalamus/ Inflammation triggers monocyte reaction

  1. Monocytes Release pyrogenic cytokines e.g. IL-1, TNFa, IL-6 into blood stream
  2. Pyrogenic cytokines stimulate endothelium of hypothalamus to release PGE2
  3. PGE2 activates EP3 receptors and downstream neurotransmitters, cAMP at Hypothalamic thermoregulatory center
  4. Increase thermoregulatory set point and activate peripheral heat response (e.g. chills, rigor)
  5. Fever
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6
Q

Define oral, rectal, tympanic and axillary temperatures limits for fever

Define hyper-pyrexia

A

Hyper-pyrexia = >40

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7
Q

Compare fever with hyperthermia

  • Physiology
  • Temperature pattern
  • Causes of hyperthermia
A

Fever:

  • Change in hypothalamic set-point by pyogenic cytokines
  • Preserve diurnal variation

Hyperthermia

  • Failure in thermoregulation
  • No diurnal variation

Causes:
Heatstroke, Malignant neuroleptic syndrome (neuroleptic, antipsychotics), Serotonin syndrome, thyroid storm

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8
Q

Causes of these fever patterns

A

A, B - Continuous fever

  • Pyogenic infections
  • Dengue fever
  • Fungal infections

C - Remittent fever

  • Infective endocarditis
  • Brucellosis
  • Typhoid fever

D - Intermittent fever

  • Malaria
  • Tuberculosis
  • Lyme disease
  • Borreliosis
  • EBV
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9
Q

Ddx major causes of fever

A

Infections: viral, bacterial, fungal, parasitic

Autoimmune diseases: e.g. Sarcoidosis, SLE, Giant cell arteritis…

Malignancies: Lymphoma, Leukaemia, RCC…

Tissue destruction: Massive infarct, Massive hemolysis, Rhabdomyolysis

Metabolic disorders: Gout attack, Porphyria

Drugs: Antibiotics, Anticonvulsants (cf hyperthermia in antipsychotics)

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10
Q

Pyrexia of unknown origin

Clinical definition

A

Fever >38.3 on several occasion
Over duration of 3 weeks
Unable to reach diagnosis despite 1 week of inpatient investigation

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11
Q

Most common causes of Pyrexia of Unknown Origin

A

Most common: Non-infectious inflammatory disorders

Infection:

  • Mycobacterial
  • Abdominal abscess
  • Endocarditis

Malignancies

  • Solid organ
  • Lymphoma

Autoimmune:

  • Vasculitis
  • Adult Still’s disease
  • SLE

Drug fever

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12
Q

4 types of hypersensitivity reactions

A
  1. IgE mediated HS
  2. IgG mediated cytotoxic HS
  3. Immune complex-mediated HS
  4. Cell-mediated HS
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13
Q

Type 1 Hypersensitivity reaction

Pathophysiology

A

IgE mediated HS

  • IgE bind to mast cells via Fc portion, allergen cross links IgE and causes degranulation
  • Causes localized and systemic anaphylaxis

E.g. seasonal allergies, food allergies

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14
Q

Type 2 Hypersensitivity reaction

  • Pathophysiology
  • example
A

IgG-mediated Cytotoxic HS

IgG tags onto target cell for:
Cytotoxic T cell recognizes Fc region of IgG and initiates cell killing (ADCC)
Complement activation

e.g. ABO mismatch, erythroblastosis fetalis

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15
Q

Type III hypersensitivity reaction

  • Pathophysiology
  • Examples
A

Immune complex mediated HS

Antigen-Ab complex deposit in tissue can activate complements, chemotaxis draws neutrophils to site of infection

Examples: Glomerulonephritis, RA, SLE

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16
Q

Type IV hypersensitivity reaction

  • Pathophysiology
  • Examples
A

Cell-mediated HS

Th1 cells secrete cytokines
Activate MQ and cytotoxic T cells to site of infection

Examples:
Contact dermatitis
Tuberculin reaction
Autoimmune diseases: Type 1 DM, Multiple sclerosis, RA

17
Q

Drug fever

3 pathophysiological mechanisms and examples of each mechanism

A

Hypersensitivity reaction

Altered thermoregulatory mechanism

  • Exogenous thyroid hormone
  • Anti-cholinergic drugs
  • Sympathomimetic drugs (e.g. ecstasy, amphetamine)

Idiosyncratic reaction (Antipsychotics and antidepressants)

  • Serotonin syndrome (SSRI, Tramadol)
  • Neuroleptic malignant syndrome
  • Malignant hyperthermia
18
Q

Outline history taking for PUO

A

Localizing symptoms: infection, malignancy, autoimmune

Drug history

  • Exogenous thyroid hormone
  • Anti-cholinergics
  • Sympathomimetics
  • Antipsychotics and antidepressants

Travel history and exposure history

Immunosuppression conditions

19
Q

2 acute phase reactants

A

Erythrocyte sedimentation rate - long-term inflammation

C-reactive protein - acute inflammation

20
Q

ESR

Confounding factors that increase and decrease ESR levels

A 
Increase ESR: 
Age 
Female sex 
Pregnancy 
Anaemia 
Renal disease

Decrease ESR:
Red cell abnormalities
Extreme leukocytosis
Hyper-viscosity (e.g. MM)

21
Q

Explain why albumin is low in acute inflammatory response (check)

A

Rouleaux formation increases during acute inflammatory response due to acute phase reactants and immunoglobulin in blood

Albumin acts to decrease the rate of rouleaux formation and becomes depleted

22
Q

C reactive protein

Physiological process of production
Function of CRP

A

Infection or inflammation activates monocytes to release IL6, IL1B

Inflammatory cytokines bind to hepatocytes and activate NFkB pathway for transcription and translation of plasma CRP

Plasma CRP increases complement C1q binding to bacterium
Plasma CRP binds to apoptotic cells for phagocytosis
Plasma CRP binds to inflamed tissue and activates neutrophil, monocytes

23
Q

Procalcitonin

Normal physiological production

A

Normal:
Only thyroid and lung produces pro-calcitonin

Thyroid C-cells produces most of pro-calcitonin and calcitonin

24
Q

Procalcitonin

  • Production during inflammation
A

Inflammation: All organs produce procalcitonin (c.f. only lung and thyroid normally)

Pathway:
LPS activates monocytes to release pro-inflammatory cytokines IL-1B and TNF-a
Pro-inflammatory cytokines active Calcitonin gene transcription in ADIPOCYTES (in any organ)
Calcitonin mRNA&raquo_space; Pro-calcitonin production
Procalcitonin directly released through vesicles from Golgi apparatus

25
Q

Compare the time of onset and concentration response of Pro-calcitonin to treatment

A

Procalcitonin level drops rapidly and rises rapidly in comparison to CRP > good for early identification of sepsis

Procalcitonin levels drop after effective treatment

26
Q

Modalities of imaging for PUO

A

CT, MRI

Gallium scan

PET-CT

MBBS VI - SpC - Family Medicine (42 decks)

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