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GP Flashcards

1
Q

What is Acne vulgaris?

A

common inflammatory disease that peaks in adolescence.
Skin condition affecting the pilosebaceous unit (hair follicle, hair shaft and sebaceous gland).
Clinically characterised by comedones, papules, pustules, nodules, cysts and/or scaring primarily on the face and trunk.
Ranges in severity from mild comedonal acne to severe nodulocystic acne which can be permanently disfiguring.
Can have psychological and social impacts on patients.

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2
Q

What is the epidemiology of Acne Vulgaris

A

Estimated 8th most common disease in the world.
Higher rates in developed countries.
Most common in boys during adolescence, more common in girls in adulthood.

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3
Q

what is the aetiology of ance vulgaris?

A

Polygenic and multifactorial
Sebaceous gland hyperplasia and excess sebum production (people with acne have larger follicle sizes and more lobules per gland, androgens cause this to happen, most prominent in puberty)
Abnormal follicular differentiation -keratinocytes are retained rather then shed as angle cells and accumulate due to their increased cohesiveness
Cutibacterium (propionibacterium) acnes colonisation - gram positive non motile rods found in follicles and stimulate production of pro-inflammatory mediators and lipases. Does Not correlate with severity
Inflammation and immune response - lead to development of papules, pustules, nodules and cysts
Around 81% down to genetics

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4
Q

what is the pathophysiology of acne vulgaris?

A

Genetic susceptibility results from variations in the pilosebaceous unit creating a environment prone to bacterial colonisation and inflammation including inherited variation in toll-like receptors (TLR-2 and 4)
Formation of the microcomedo
Retention and accumulation of keratinocytes
Androgens stimulate enlargement of the sebaceous gland and increased sebum production collecting in the microcomedo
Leads to a buildup of pressure and whorled lamellar concretion develop
This allows the proliferation of c acnes producing pro inflammatory mediators
Microcomedo may rupture and release immunogenic keratin and sebum, stimulating a further inflammatory response
Suppurative pustules or inflamed papules, nodule or cysts then may develop
Post inflammatory hyperpigmentation and scarring may result

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5
Q

what are the risk factors for acne vulgaris?

A

Age 12-24 years
Genetic predisposition
Greasy skin and increased sebum production
Medications - androgens, corticosteroids, antiepileptic, isoniazid, lithium and adrenocorticotropic hormone
Endocrine disorders
Diet
Female / oestrogen
Obesity
Hyperandrogenism
Halogenated aromatic hydrocarbons exposure

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6
Q

what are the key presentation of acne?

A

Presence of above risk factors
Skin lesions - open and close comedone (non inflammatory), papules, pustules, nodules and cysts (inflammatory)
Post inflammatory scarring
Skin tenderness
Depression or social isolation

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7
Q

what are the differential for acne vulgaris?

A

Acne keloidalis nuchae
Acneiform eruptions
Chloracne
Favre-racouchot syndrome
Folliculitis
Gram negative folliculitis
Lupus miliaris disseminatus faciei
milia

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8
Q

how is acne vulgars treated?

A

Mild no inflammation - topical retinoid or salicylic acid, benzoyl peroxide
Mild with inflammation - topical retinoid or topical antibiotic, benzoyl peroxide, azelaic acid, topical dapsone
Moderate no inflammation - as mild but 2nd line add dapsone
Severe or resistant - oral retinoid, consider oral corticosteroid
If hormone related - oral hormone therapy
Pregnant - topical antibiotic

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9
Q

what is the recommended monitoring for acne vulgaris?

A

Monitor liver is on isotretinoin

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10
Q

what are the complications of acne vulgaris?

A

Scarring
Dyspigmentation

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11
Q

what is the prognosis of acne vulgaris?

A

Typically improves on people progressing through adolescence, may persist into adulthood
Servere lesions may leave scaring
Peeling or dryness may occur form topical treatments

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12
Q

how is acne vulgaris investigated?

A

clinical diagnosis is first line and gold standard

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13
Q

what is acute bronchitis?

A

Self limiting lower respiratory tract infection.
Infection causing inflammation to the bronchial airways.
Acute illness (<21 days)
Cough as predominant symptom
At least 1 other LRT symptom - sputum, wheeze, chest pain
No alternative explanation for symptoms

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14
Q

what is the epidemiology of acute bronchitis?

A

Highest incidence in autumn and winter

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15
Q

what is the aetiology of acute bronchitis?

A

Most cases are viral - coronavirus, rhinovirus, RSV, adenovirus
Younger populations of military recruits and college students - Chlamydia pneumoniae and Mycoplasma pneumoniae (very rare)
Immunocompromised may be caused by Bordetella bronchiseptica (very rare)

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16
Q

what are the risk factors for acute bronchitis?

A

Viral or atypical bacterial infection exposure - Seasonal or close contacts
Cigarette smoking
Household pollution exposure

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17
Q

what is the pathophysiology of acute bronchitis?

A

Acute inflammation of the bronchial wall causing increased mucus production together with oedema of the bronchus. Leads to a productive cough.
Repair of the bronchial walls may take several weeks and patients may continue to cough during this time
Patients exhibit similar bronchial obstruction to asthma, pulmonary function return to normal after symptoms abate
Cough >1 month = post-bronchitis syndrome

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18
Q

what is the key presentation of acute bronchitis?

A

Presence of above risk factors
Cough <30 days
Productive cough
No history of chronic respiratory illness
Exclusion of other respiratory and cardiac illnesses
Fever
Wheezes
rhonchi

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19
Q

how is acute bronchitis investigated?

A

first line and gold standard is clinical diagnosis by ruling out other causes through
pulmonary function tests
CXR
CRP

20
Q

what are the differentials for acute bronchitis?

A

COVID 19
Pneumonia
Allergic rhinitis
Asthma
Pertussis infection
CHF
Reflux oesophagitis
Upper respiratory infection
Upper airway cough
Medication or environment exposure
Lung cancer

21
Q

how is acute bronchitis managed?

A

Cough <4 weeks:
Observation, antipyretic (paracetamol), SABA, antitussive (dextromethorphan), antibiotics
Cough >4 weeks:
Evaluate other causes, SABA

22
Q

how is acute bronchitis monitored?

A

Rarely necessary
Patients with ongoing symptoms - evaluate for other causes

23
Q

what are the complications of acute bronchitis?

A

Chronic cough
Pneumonia

24
Q

what is the prognosis of acute bronchitis?

A

Most recover within 6 weeks
Recurrence is common, especially with smokers

25
Q

what is the epidemiology of B12 anaemia?

A
  • The disease is common in the elderly (over 60)
  • Seen in all races but more common in fair-haired, blue eyed individuals and those who have blood group A
  • More common in FEMALES than males
  • There is also an association with other autoimmune disease such as thyroid disease and Addison’s disease
26
Q

what is the aetiology of B12 anaemia?

A

Pernicious anaemia (autoimmune gastric atrophy; loss of intrinsic factor production)
gastrectomy/ ileal resection
vegan diet
bacterial overgrowth
oral contraceptives
hypochloridia
Recreational nitric oxide use

27
Q

what are the risk factors for B12 anaemia?

A
  • Veganism (exclusively found in meat and dairy products)
  • Elderly
  • Female
  • Fair-haired, blue eyes
  • Blood group A
  • Thyroid and Addison’s disease
  • stomach removed
28
Q

what is the pathophysiology of B12 anaemia?

A

Pernicious anaemia is an AUTOIMMUNE DISORDER in which the parietal cells of the stomach are attacked resulting in atrophic gastritis and the loss of intrinsic factor production and thus vitamin B12 malabsorption
Thus in B12 deficiency there is an impairment of DNA synthesis resulting in delayed nuclear maturation resulting in large RBCs as well as decreased RBC production in the bone marrow
- This DNA impairment will affect all cells, but bone marrow is most affected since it’s the most active in terms of cell division

29
Q

what is the key presentation of B12 anaemia?

A

Onset is insidious with progressively increasing symptoms of anaemia, lemony yellow coloured skin (due to pallor and jaundice), red sore tongue, neurological features

Fatigue, headache, dyspnea, palpitations, pallor, yellowy skin, red sore tongue, ulcerations on corners of mouth
Neurological - paresthesia (symmetrical burning in fingers and toes), loss of proprioception, weakness and ataxia, paraplegia, hallucinations

30
Q

how is vitamin B12 deficiency diagnosed?

A

-FBC - macrocytic (high MCV), low haematocrit and haemoglobin
-peripheral blood smear - oval macrocytes with hypersegmanted neutrophil polymorphhs with 6 or more lobes in the nucleus
- Serum bilirubin may be raised as a result of ineffective erythropoiesis resulting in increased RBC breakdown
- Serum B12 is low
- Reticulocyte count is LOW
- Intrinsic factor antibodies - DIAGNOSTIC of pernicious anaemua but lower sensitivity i.e. not present in all patients

31
Q

what are the differentials for B12 anaemia?

A

folic acid deficiency
MDS
alcoholic liver disease
hypothyroidism
peripheral neuropathy
diabetic neuropathy
drug induced macrocytosis
dementia
depression

32
Q

how is B12 deficiency managed?

A
  • In combined B12 and folate deficiency, ensure B12 started before folate
  • If not pernicious anaemia then treat cause
  • If a low B12 is due to malabsorption then injections are required
  • If cause is dietary then give oral B12
  • Replenish B12 stores by giving IM HYDROXOCOBALAMIN
33
Q

how is B12 anaemia monitored?

A

Patients with vitamin B12 deficiency should have close follow-up to confirm the diagnosis and to determine response to treatment. In patients with minimal symptoms and without anaemia causing haemodynamic compromise, this can generally be done 2 to 3 months from initiation of treatment. Follow-up serum vitamin B12 levels, methylmalonic acid levels, or homocysteine levels should be measured to determine response to treatment.

34
Q

what are the complications of B12 anaemia?

A

neurological deficits - paraesthesia, ataxia, peripheral neuropathy, memory loss, vision loss
haemtological deficits - anaemia, thrombocytopenia, leukopenia
gastric cancer
low birth weight with preterm delivery

35
Q

what is the prognosis of B12 anaemia?

A

Vitamin B12 deficiency can cause devastating neurological disease and severe haematological disorders. Early diagnosis and prompt treatment may halt progression and reverse neurological disease.
Unfortunately, many cases are irreversible and clinical disease may not respond to adequate therapy.
Early diagnosis in the near-asymptomatic stage can be critical in preventing permanent neurological damage.

36
Q

what is the definition of folate anaemia?

A

Megaloblastic anaemia without neuropathy is the classic manifestation of folate deficiency

37
Q

what is the epidemiology of folate deficiency?

A

higher rates in countries without fortification of foods such as breakfast cereals

38
Q

what is the aetiology of Folate deficiency?

A

Main cause is poor intake e.g. poverty, alcoholics and elderly
Increased demand e.g. pregnancy or increased cell turnover i.e.=haemolysis, malignancy, inflammatory disease and renal dialysis
Malabsorption e.g. coeliac disease or Crohn’s disease
Antifolate drugs e.g. methotrexate and trimethoprim

39
Q

what are the risk factors for folate anaemia?

A
  • Poor nutrition, malabsorption
  • Elderly
  • Poverty
  • Alcoholic
  • Pregnant
  • Crohn’s or coeliac disease
40
Q

what is the pathophysiology of folate anaemia?

A

Folate deficiency there is an impairment of DNA synthesis resulting in delayed nuclear maturation resulting in large RBCs as well as decreased RBC production in the bone marrow
- This DNA impairment will affect all cells, but bone marrow is most affected since it’s the most active in terms of cell division
- Folate is also essential for foetal development - deficiency can result in neural tube defects

Most dietary folate is metabolised to 5-methyl-tetrahydrofolate (5-methyl-THF) when it crosses the intestinal mucosa. When 5-methyl-THF enters the cells in the body, it is catalysed to tetrahydrofolate by the vitamin B12-dependent enzyme methionine synthase. THF is then polyglutamated (by the enzyme folylpolyglutamate synthetase) and retained in the cell.
Folate, in its reduced form tetrahydrofolate, is a 1-carbon transporter that serves as an essential co-enzyme for three key intracellular processes involved in cell viability and growth: DNA synthesis and repair, methylation reactions, and dihydronicotinamide adenine dinucleotide phosphate (NADPH) generation.

41
Q

what are the key presentations of folate anaemia?

A

Patients may be asymptomatic
- May present with symptoms of anaemia e.g. pallor, fatigue, dyspnoea, anorexia and headache
- Glossitis (red sore tongue) can occur
- NO NEUROPATHY unlike B12 deficiency - how you can differentiate

42
Q

how is folate anaemia diagnosed?

A

blood smear - macrocytosis, anisocytosis, poikilocytosis, hypersegmented neutrophils
FBC - low haemoglobin, elevated MCV and MCH; increased MCV and MCH may be absent or less than expected in combined folate and iron deficiency; thrombocytopenia, neutropenia
reticulocyte count - low corrected reticulocyte ount

43
Q

how is folate anaemia treated?

A

Replace orally. Do not replace folate without checking B12
- Treat underlying cause
- Give FOLIC ACID TABLETS daily for 4 months - NEVER WITHOUT B12 as well (unless the patient is known to have NORMAL B12) since in low B12 states it may precipitate/worsen subacute combined degeneration of the spinal cord

44
Q

how is folate anaemia monitored?

A

Reticulocytosis can be assessed at the end of the first week of therapy. It is important to determine completeness of response after 8 weeks of therapy, when blood counts should have normalised.

Homocysteine levels fall within a few days of therapy and may be used to assess treatment response.

Inadequate response indicates a co-existing cause of anaemia, such as iron deficiency or vitamin B12 (cobalamin) deficiency.

45
Q

what are the complications of folate anaemia?

A

Infertility, CVD, cancer, problems in childbirth, neural tube defects, low WBC counts

Phase 3a (6 decks)

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