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General Practice Flashcards

1
Q

What is the pathophysiology of acne vulgaris?

A
  • Chronic inflammation with or without localised infection in the pilosebaceous unit
  • Increased production of sebum, trapping of keratin (dead skin cells) and blockage of the pilosebaceous unit. - Swelling and inflammation in a unit = comedones
  • Androgenic hormones increase the production of sebum
  • Propionibacterium acnes bacteria has a big role
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2
Q

Causes of acne vulgaris?

A
  • Mainly due to excess androgen
  • Endogenous causes include PCOS or congenital adreal hyperplasia
  • Exogenous = steroids, antiepileptics, epidermal growth factor receptor inhibitors
  • Occlusion of pilosebaceous unit such as shaving or cosmetic products
  • Chemicals - occupational acne
  • High glycaemic index foods and dairy products
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3
Q

What are the options for topical management of acne vulgaris?

A
  • Aims are to reduce symptoms, reduce risk of scarring and reduce psychosocial impact. Always investigate potential associated anxiety and depression
  • Salicyclic acid
  • Topical benzoyl peroxide
  • Topical retinoids but women of childbearing age need contraception as it’s teratogenic
  • Topical antibiotics like clindamycin
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4
Q

What are the options for systemic management of acne vulgaris?

A
  • Oral antibiotics like tetrecyclines e.g. lymecycline
  • Combined oral contraceptive pill
  • Spironolactone
  • Oral Retinoids - highly teratogenic
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5
Q

What is the most effective option for COCP when managing acne?

A

Co-cyprindiol (Dianette) is the most effective but there is a higher risk of VTE, so treatment is stopped once acne is controlled and it is not prescribed long term

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6
Q

What are the side effects of isotretinoin (Roaccutane)?

A
  • Strongly teratogenic - need to stop at least a moth before getting pregnant
  • Dry skin and lips
  • Photosensitivity of the skin to sunlight
  • Depression, anxiety, aggression and suicidal ideation so patients should be screened for mental health issues prior to starting treatment.
  • Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
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7
Q

What is the pathophysiology of acute bronchitis?

A

Temporary inflammation of the airways caused by a virus which causes a cough and mucus production. It lasts up to 3 weeks and is more common in children under 5.

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8
Q

How does acute bronchitis present?

A
  • Hacking cough that may bring up yellow/grey/clear/green mucus
  • Sore throat
  • Headache
  • Runny or blocked nose
  • Myalgia
  • Fatigue
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9
Q

How to investigate acute bronchitis?

A

This is usually a clinical diagnosis

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10
Q

How do you manage acute bronchitis? When should you see a GP?

A
  • rest, hydration and NSAIDs
  • see a GP if your cough lasts longer than 3 weeks
  • high temp for over 3 days
  • if you cough up mucus streaked with blood
  • if you have a heart or lung condition
  • if you develop chest pain or SOB
  • only prescribe Abx for people at risk of developing pneumonia (1/20 cases) e.g. premature babies, age over 80, history of heart/lung/kidney/liver disease, immunocompromised or CF - if Abx prescribed it’s usually 5 days of amoxicillin or doxycyline
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11
Q

What is an acute stress reaction?

A

A severe stress reaction to an unexpected life crisis. Can last hours to 2/3 days.

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12
Q

How does an acute stress reaction present?

A
  • Psychological - anxiety, low mood, irritability, poor sleep etc
  • dreams or flashbacks
  • aggressive behaviour
  • avoidance of triggers
  • emotional numbness/isolation
  • physical - palpitations, nausea, chest pain, headache, abdo pain, SOB
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13
Q

How would you manage acute stress reaction?

A

A reaction usually resolves in a few days but if this lasts longer than that and up to a month then it is classed as acute stress disorder. This is a psychiatric disorder and needs the input of mental health professional and psychological therapies.

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14
Q

What is anaemia? What are the types of anaemia?

A

Reduced haemoglobin results in impaired oxygen delivery to the body - defined as 2 standard deviations below what is normal for their age and sex - 130g/L for men and 120g/L for women. Classified by the size of the RBC - mean corpuscular volume:

Microcytic anaemia: MCV < 80
Normocytic anaemia: MCV 80 – 100
Macrocytic anaemia: MCV >100

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15
Q

What are the causes of microcytic anaemia?

A

T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia

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16
Q

What are the causes of normocytic anaemia?

A

A – Acute blood loss
A – Anaemia of Chronic Disease
A – Aplastic Anaemia
H – Haemolytic Anaemia
H – Hypothyroidism

e.g. hereditary spherocytosis, sickle cell anaemia , glucose 6 phosphate dehydrogenase deficiency, immune haemolytic anaemia, microangiopathic haemolytic anaemia, paroxysmal nocturnal haemoglobinuria

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17
Q

What are the types of macrocytic anaemia?

A
  • megaloblastic anaemia is due to impaired DNA synthesis so they are large immature RBCs
  • non-megaloblastic is not caused by impaired DNA synthesis but still produces large RBCs
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18
Q

What are the causes of macrocytic anaemia?

A

folate deficiency
B12 deficiency
alcoholism
liver disease
reticulocytosis
hypothyroidism
haem malignancies

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19
Q

How does anaemia present?

A

Pallor, Fatigue, Breathlessness, Dizziness, Palpitations, Cold hands and feet, pica + hair loss in iron deficiency

Also screen for: malnutrition, malabsorption (gastrectomy or coeliac), blood loss, black tarry stools, family history, underlying chronic disease

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20
Q

What are the causes of iron deficiency anaemia?

A
  • blood loss - GORD, ulcers, IBD, malignancy, hookworm/schistosomiasis and NSAIDs
  • dietary deficiency
  • poor absorption
  • increased requirement during pregnancy
  • PPI - reduce acidity of stomach so iron becomes insoluble and can’t be absorbed
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21
Q

What investigations do you do for iron deficiency anaemia?

A
  • FBC - shows low Hb and MCV, reduced mean corpuscular haemoglobin
  • Ferritin - be careful as it is an acute phase reactant and goes up during inflammation
  • Low transferrin saturation
  • Raised total iron-binding capacity (TIBC)
  • Blood film - hypochromic cells (pale), anisocytosis (different sizes) ad poikilocytosis (different shapes)
  • B12 and Folate
  • If no clear cause then check for underlying causes - coeliac serology (anti ttg), stool sample (IBD, parasites), urine dipstick for haematuria, GI investigations in 60+, FH of GI cancer, treatment resistant anaemia and premenopausal women with bowel symptoms
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22
Q

How does iron deficiency anaemia present?

A

Dyspnoea, fatigue, headache, palpitations, pale skin or conjunctiva, restless leg syndrome, pica (a craving non-food substances, such as ice or dirt – commonly seen in children and pregnant women), tinnitus, pruritus, hair loss, mouth ulcers, vertigo/dizziness, angular chelitis, atrophic glossitis, angular stomatits, koilonychia, dry skin and hair

Also symptoms of underlying disease such as dysphagia, dyspepsia, abdo pain, change in bowel habit, rectal bleeding and weight loss

Also check last menstrual period and NSAID use

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23
Q

How do you manage anaemia?

A

From fastest to slowest:
- Blood transfusion - immediately corrects but does not correct the cause and has risks
- Iron infusion e.g. “cosmofer”- small risk of anaphylaxis but it quickly corrects it, avoid during sepsis as iron “feeds” bacteria
- Oral iron e.g. ferrous sulfate - slowly corrects the iron deficiency but causes constipation and black coloured stools. It is unsuitable where malabsorption is the cause of the anaemia

When correcting iron deficiency anaemia with iron you can expect the haemoglobin to rise by around 10 grams/litre per week.

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24
Q

What is sideroblastic anaemia?

A

Characterised by defective protoporphyrin synthesis which can be congenital (ALAS deficiency) or acquired because of alcoholism, lead poisoning or vitamin B6 deficiency.

Basically the iron is fine but can’t form haem so then iron builds up in the mitochondria creating the pathognomonic sideroblasts

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25
Q

What is thalassemia?
- types, presentation, Ix, management and inheritance

A
  • A type of microcytic anaemia due to an inherited gene mutation affecting globin
  • Can be alpha (16) or beta (11) and categorised by how severe it is
  • Pronounced forehead and malar eminences due to extramedullary erythropoiesis
  • Diagnosed with FBC, Hb electrophoresis and genetic testing
  • Management depends on severity
  • Autosomal recessive
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26
Q

What is Haemoglobin H disease and what is Hb Barts disease?

A

These are subtypes of alpha thalassaemia. It is categorised by how many normal copies of globin genes you have:
- aa/a- = minima = asymptomatic
- aa/– = trait = mild anaemia
- a-/– = HbH disease = haemolytic anaemia
- –/– = Hb Barts = still born baby as this is incompatible with extrauterine life - Hydrops Fetalis due to 4 gammas

HbH is hypochromic and microcytic RBCs which get removed quickly by the spleen, are more prone to oxidative stress and have a higher affinity for oxygen than normal Hb so do not deliver it to tissues

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27
Q

What are the types of Hb?

A
  • HbA: two alpha, two beta (95-98% in adults)
  • HbA2: two alpha, two delta (2-4% in adults)
  • HbF: two alpha, two gamma
  • Gower: two zeta, two epsilon (embryonic haemoglobin)
    Portland: two zeta, two gamma (embryonic haemoglobin)
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28
Q

What is the pathophysiology of anaemia of chronic disease?

A

An underlying chronic disease such as malignancy, chronic infections, or autoimmune conditions, causes the liver to produce acute phase reactants such as hepcidin.

Hepcidin “hides” the iron in ferritin to reduce availability in the serum. Anaemia of chronic disease starts out as normocytic anaemia but it can progress to microcytic anaemia.

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29
Q

What is hereditary spherocytosis? Pathophysiology, Ix and Tx

A

Autosomal dominant inherited defect of RBC cytoskeleton membrane proteins such as ankyrin and spectrin. Because of abnormal structure they can’t move through the spleen so they get stuck and haemolyse.

You get increased reticulocytes because the body tries to compensate for the increased levels of extravascular haemolysis. Also get low Hb, high uric acid (haemolysis) and blood film shows spherocytes.

Many patients manage fine but if needed then the treatment of choice is a splenectomy

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30
Q

Which genetic mutation causes sickle cell anaemia?

A

An autosomal recessive mutation on chromosome 11 in the beta-globin chain of haemoglobin, causing valine to replace glutamic acid (because tyrosine becomes adenine)

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31
Q

What is the pathophysiology of sickle cell anaemia?

A

When RBCs with HBS undergo physiological stress such as low oxygen they polymerise and become sickled so they stick together and cause vaso-occlusive crises. They also undergo haemolysis so they have a shorter lifespan of 10-20 days instead of 120.

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32
Q

Which physiological stressors can cause a sickle cell crisis?

A

Hypoxia
Dehydration
Infection
Cold temperatures
Acidosis (e.g. lactic acidosis following exertion)

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33
Q

What are the complications of vaso-occlusion?

A

Acute painful episodes (i.e. painful crisis)
Acute chest syndrome (i.e. chest crisis)
Renal infarction
Bone infarction or dactylitis (inflammation of a digit)
Myocardial infarction
Stroke
Venous thromboembolism
Priapism (persistent, painful erection)

34
Q

What is an aplastic crisis and what causes it in sickle cell anaemia?

A
  • Temporary cessation of erythropoiesis, causing severe anaemia
  • Usually precipitated by infection with parvovirus B19
  • Patients may present with high-output congestive heart failure secondary to anaemia
  • Usually need a transfusion
35
Q

How is sickle cell anaemia diagnosed?

A
  • Testing is offered during pregnancy
  • Tested for in the newborn heelprick test at 5 days old
  • FBC shows low Hb
  • Blood film shows sickled cells and features of hyposplenism such as target cells and Howell-Jolly Bodies
  • Sickle solubility test - mix with sodium dithionite and HbS will make it go turbid as a precipitate forms whereas normal blood goes clear
  • ## Hb Electrophoresis - need to diagnose SCA
36
Q

How do you manage sickle cell anaemia long term?

A
  • Avoid triggers
  • Prophylaxis for infection with oral penicillin until at least the age of 5
  • Make sure they are fully vaccinated plus vaccinations against meningococcus, pneumococcus, hepatitis B and influenza
  • Folic acid supplements
  • Transfusion plus iron chelation therapy
  • Hydroxycarbamide increases HbF
  • Allogenic bone marrow transplant - can be curative but very difficult to find a match
37
Q

How do you manage a vaso-occlusive crisis?

A
  • Analgesia, warmth, rest and rehydration
  • If severe then admit for opioids and screen for trigger such as infection - adequate analgesia is essential to avoid atelectasis
  • Manage complications
38
Q

What is the pathophysiology of G6PD Deficiency?

A

If cells are lacking in glucose 6 phosphate dehydrogenase then they are more prone to oxidative stress. G6PD makes NADPH, which in turn creates reduced glutathione to protect the cell from oxidative injury. This leads to intravascular haemolysis via oxidative stress.

39
Q

How is G6PD deficiency inherited?

A

X linked inheritance so mainly affects men

40
Q

How does G6PD deficiency present?

A
  • Usually asymptomatic but when exposed to certain triggers such as antimalarial drugs they experience episodes of anaemia
  • When exposed to oxidative stress they may experience lethargy, dizziness, SOB, jaundice, dark urine, abdo/back pain, pallor, jaundice, splenomegaly
41
Q

What are some triggers for G6PD?

A
  • Antibiotics: nitrofurantoin, fluoroquinolones, sulphonamides
  • Antimalarials: primaquine, chloroquine (possible), quinine (possible)
  • Other: Dapsone, Methylene blue, Sulfonylureas, Rasburicase
  • Fava beans
  • Illness and infection
42
Q

How do you diagnose G6PD?

A

Main Ix is test for the G6PD enzyme plus FBC, high reticulocyte count, LFT just unconjugated bilirubin, reduced haptoglobin, blood film shows cell fragments and Heinz bodies, direct antiglobulin test is negative

43
Q

How do you manage G6PD Deficiency?

A

Avoid precipitants of oxidative stress
In acute haemolysis the may need a transfusion
Chronic anaemia may require folic acid supplements

44
Q

What is immune mediated haemolytic anaemia?

A

When antibodies bind to parts of the RBC membrane which can lead to fixing of a complement and phagocytosis by a macrophage. It can have alloantibodies (transfusion reactions or haemolytic disease of the newborn) or autoantibodies (AIHA).

45
Q

What is warm autoimmune haemolytic anaemia?

A

When antibodies react with RBC at a higher temperature (above 37) leading to agglutination. Can be idiopathic or secondary to infections such as HIV and EBV, inflammatory disorders such as SLE, or malignancies such as chronic lymphocytic leukaemia and non-Hodgkin’s lymphoma

46
Q

What is cold autoimmune haemolytic anaemia?

A

a reaction against RBCs at lower temperatures (e.g. < 32°), which then leads to agglutination. Cold AIHA may be idiopathic or associated with systemic diseases such as lymphoma, Mycoplasma pneumoniae infection and infectious mononucleosis

47
Q

How do you diagnose AIHA?

A

Direct Coombs test using antiglobulin

48
Q

What is microangiopathic haemolytic anaemia?

A

RBCs are destroyed because of structural issues with the vasculature, such as microthrombi, prosthetic heart valves and aortic stenosis. Sometimes the RBCs get torn on these protruding structures, creating visibly distinct schistocytes.

Can also be secondary to:
- Haemolytic Uraemic Syndrome (HUS)
- Disseminated Intravascular Coagulation (DIC)
- Thrombotic Thrombocytopenia Purpura (TTP)
- Systemic Lupus Erythematosus (SLE)
- Cancer

49
Q

How do you manage AIHA?

A

Blood transfusions
Prednisolone (steroids)
Rituximab (a monoclonal antibody against B cells)
Splenectomy

50
Q

What is Paroxysmal Nocturnal Haemoglobinuria?

A

It’s a rare condition that occurs when a specific genetic mutation in the haematopoietic stem cells in the bone barrow happens resulting in loss of proteins on the surface of RBCs that inhibits the complement cascade.

So because they’re missing the proteins to inhibit complements it activates the complement cascade and the RBCs get destroyed.

51
Q

How does paroxysmal nocturnal haemoglobinuria present and how do you manage it?

A

Red urine in the morning containing haemoglobin and haemosiderin and anaemia. Also predisposed to VTE and smooth muscle dystonia.

Management is with eculizumab or bone marrow transplantation. Eculizumab is a monoclonal antibody that targets complement component 5 (C5) causing suppression of the complement system. Bone marrow transplantation can be curative.

52
Q

What is folate deficiency and how do you diagnose it?

A

Folate deficiency can be caused by many things such as poor diet, alcoholism, antifolate drugs, haemolytic anaemias and pregnancy. It causes megaloblastic anaemia.

High MCV, high homocysteine, normal methylmalonic acid

53
Q

What is pernicious anaemia?

A

In order for B12 to be absorbed in the terminal ileum it needs to bind to intrinsic factor which is made by the parietal cells in the stomach. In pernicious anaemia there is autoimmune destruction of the parietal cells or intrinsic factor so B12 can’t be absorbed.

54
Q

What are the causes of B12 deficiency?

A
  • pernicious anaemia
  • pancreatic insufficiency
  • dietary deficiency
  • damage to terminal ileum
55
Q

How do you diagnose pernicious anaemia?

A
  • Intrinsic factor antibody is the first line investigation
  • Gastric parietal cell antibody can also be tested but is less helpful
56
Q

What is the main difference between presentation of B12 deficiency and folate deficiency?

A

B12 deficiency has neurological disturbance because there is increased methylmalonic acid (in folate it is normal and only homocysteine is increased whereas in B12 both are high)

57
Q

How do the neurological symptoms of pernicious anaemia present?

A
  • Peripheral neuropathy with numbness or paraesthesia (pins and needles)
  • Loss of vibration sense or proprioception
  • Visual changes
  • Mood or cognitive changes
58
Q

If there is concurrent B12 and Folate deficiency what do you treat first and why?

A

If there is B12 and folate deficiency it is important to treat the B12 deficiency first before correcting the folate deficiency. Treating patients with folic acid when they have a B12 deficiency can lead to subacute combined degeneration of the spinal cord.

59
Q

How do you treat B12 deficiency?

A
  • dietary deficiency can be treated with oral cyanocobalamin
  • in pernicious anaemia it’s 1mg hydroxycobalamin 3x a week for 2 weeks and then every 3 months, may need a more intense regimen if there are neurological symptoms
60
Q

What is an anal fissure?

A

A tear in the mucosal lining of the anal canal, most commonly due to trauma from defecation of hard stool. It can be classified according to its duration. Acute is less than 6 weeks and chronic is longer than 6 weeks.

61
Q

What are causes of anal fissures?

A

Primary - no clear cause
Secondary causes:
- Constipation
- IBD
- Malignancy (e.g. squamous cell anal cancer)
- Sexually transmitted infections (e.g. HIV, syphilis)
- Infections (e.g. bacteria, fungal, viral)
- Anal trauma (e.g. anal sex)
- Pregnancy and childbirth

62
Q

Where are anal fissures usually located?

A

Posterior midline of the anal canal within the anoderm because this area has the least blood supply, in childbirth it happens anteriorly

*the anoderm is the epithelium located distal to the dentate line for approximately 1.5 cm

63
Q

How do anal fissures present?

A
  • pain on defecation
  • PR bleeding
  • DRE may be too painful to perform
  • tear may be visible
  • skin tags are a sign of chronic fissures
  • itching
64
Q

How do you diagnose anal fissures?

A

Normally a clinical diagnosis that can be confirmed with visualisation but be wary of an underlying cause e.g. crohn’s disease and also remember that fissures are uncommon in the elderly so have a low threshold for investigating for malignancy

  • can also do examination under anaesthesia and proctoscopy
65
Q

How do you manage anal fissures?

A
  • Reduce risk factors so advise patients to increase dietary fibre, drink water and eat a balanced diet
  • Stool softening laxatives such as lactulose or movicol
  • Analgesia but do not give opioids
  • 5% lidocaine ointment
  • GTN cream or diltiazem cream - increases the blood supply to the region and relaxes the internal anal sphincter, putting less pressure on the fissure
  • Surgery when symptoms persist for at least 8 weeks
  • Botox injections into internal anal sphincter
66
Q

What are the surgical management options for anal fissures?

A

Lateral internal sphincterotomy
Botox injection
Fissurectomy
Anal advancement flap

67
Q

What is anaphylaxis?

A

A systemic type 1 hypersensitivity reaction mediated by IgE which stimulates mast cells to degranulate and release pro-inflammatory chemicals such as histamine causing airway/breathing/circulation + skin and mucosal changes. NB it can sometimes be non-immunological.

68
Q

What differentiates between an anaphylactic and non-anaphylactic allergic reaction?

A

The key feature that differentiates anaphylaxis from a non-anaphylactic allergic reaction is compromise of the airway, breathing or circulation. Skin and mucosal changes alone do not indicate anaphylaxis as 20% of these cases will not have such symptoms.

69
Q

What is mortality and incdence in anaphylaxis?

A

Mortality is less than 1% in patients presenting to hospital and approximately 1 in 300 people will have it in their lifetime whilst 1 in 12 will have recurrent anaphylaxis

70
Q

What is an allergy?

A

An exaggerated immune response to an otherwise innocuous substance

71
Q

What is sensitisation in an allergy?

A

When an allergen enters the body and is taken up by an antigen presenting cell which interacts with a t helper cell (Th2) which stimulate B cells in lymphoid tissue to produce IgE which then stimulates mast cells and basophils

72
Q

How does anaphylaxis present?

A

Throat/tongue swelling
Horse voice
Stridor
Dyspnoea
Wheeze
Hypoxia
Persistent cough
Respiratory arrest
Pale, clammy
Dizziness
Tachycardia
Hypotension
Cardiac arrest
Reduced Glasgow coma score (GCS)
Agitation
Confusion
‘Feeling of impending doom’
Urticaria
Angio-oedema
Nausea, D + V, Abdo pain

73
Q

What is the emergency management of anaphylaxis?

A
  • Secure the airway
  • Provide oxygen if required. Salbutamol can help with wheezing.
  • Provide an IV bolus of fluids
  • Lie the patient flat to improve cerebral perfusion
  • Look for flushing, urticaria and angio-oedema

Intramuscular adrenalin, repeated after 5 minutes if required
Antihistamines, such as oral chlorphenamine or cetirizine
Steroids, usually intravenous hydrocortisone

74
Q

Which protein plays an important role in anaphylaxis but is not useful in initial diagnosis or management of it?

A

Mast cell tryptase

Take at least one sample 1-2 hours after onset and 6 hours max but do not let this delay any treatment. Ideally take 1 sample at onset, one 1-2 hours after and one taken at least 24 hours later as a baseline measurement.

Sometime it isn’t always raised on anaphylaxis but can be important in differentiating anaphylaxis from conditions that mimic it such as hereditary angio-oedema

75
Q

Which guidelines should you follow for emergency treatment of anaphylaxis?

A

Resuscitation council guidelines 2021

76
Q

Where should emergency IM adrenalin be administered? What concentration?

A

Anterolateral aspect of the anterior thigh. Conc should be 1mg/ml

77
Q

What dose of adrenalin should be administered in anaphylaxis?

A
  • Adult and child >12 years old: 500 micrograms IM
  • 6-12 years old: 300 micrograms IM
  • 6 months - 6 years: 150 micrograms IM
  • < 6 months: 100-150 micrograms
78
Q

How does adrenalin work in anaphylaxis?

A
  1. Alpha-adrenergic receptors: causes vasoconstriction that reverses peripheral vasodilation and reduces tissue oedema
  2. Beta-adrenergic receptors: causes bronchodilation, increases myocardial contractility and suppresses histamine/leukotriene release. Also inhibits mast cell activation
79
Q

What is refractory anaphylaxis?

A

Defined as anaphylaxis requiring ongoing treatment despite two appropriate doses of adrenaline

Refer to critical care, they will give infusion of adrenalin and keep giving IM adrenalin at 5 minute intervals whilst infusion is being prepared as well as ongoing fluid resus

80
Q

What is a biphasic reaction?

A

Recurrence of symptoms of anaphylaxis several hours later in the absence of exposure to the allergen.

Around 5% of patients will get this at a mean time of 12 hours

RF for it:
- Severe initial presentation
- More than one dose of adrenaline required
- Delay in giving adrenaline

81
Q

What steps should be taken to manage anaphylaxis after a patient is stable?

A
  1. Review by senior clinician
  2. Patient info on avoiding triggers, basic life support for parents and how to use an auto-injector
  3. Adrenaline auto-injector should be prescribed, patients should have 2 at least
  4. Refer to allergy/immunology clinic where they will have allergen specific IgE antibodies testing and skin testing

med (9 decks)

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