Cardiovascular, Blood, Infectious diseases, HIV/AIDS, Diabetes, Red Flags Flashcards

1
Q

What are the infective inflammatory conditions of the heart?

A

Endocarditis: Inflammation of heart valves due to infection by bacteria or fungi

Myocarditis: Inflammation of heart muscle due to many causes but most commonly viral attack

Pericarditis: Inflammation of pericardium due to many causes but commonly bacterial infection

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2
Q

What are the clinical signs and symptoms of myocarditis?

A

May develop along with cold/chest infection

Symptoms include fever, fatigue, chest pain, arrhythmias AND Joint pain and swelling (leg swelling common)

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3
Q

What are the clinical signs and symptoms of pericarditis?

A

Inner surfaces of pericardium become adhesive and can be auscultated as a rub
Oedema often results leading to fluid build up around heart (Tamponade)
Often associated with auto-immune conditions such as lupus AND rheumatoid arthritis

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4
Q

What are the pathophysiology and clinical signs and symptoms of endocarditis?

A

Vegetations (clumps of bacteria and cells) form on the heart valves – may cause valve destruction, regurgitation or obstruction.

Bacteria may gain entry from dental or medical procedure, respiratory infection, urinary tract infection or fracture

Signs and symptoms:

Fever/chills/ night sweats/excessive sweating
Fatigue & Shortness of breath with activity
Heart murmur
Joint pain/muscle aches and pains
Nail abnormalities (splinter hemorrhages under the nails)
Red, painless skin spots on the palms and soles (Janeway lesions)
Red, painful nodes in the pads of fingers/toes (Osler’s nodes)
Abnormal urine color & blood in the urine
Paleness
Swelling of feet, legs, abdomen
Weakness
Weight loss

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5
Q

What are arrhythmias?

A

If synchronization of cardiac muscle contraction is disrupted uncoordinated contraction known as fibrillation can result.
This may be a group of symptoms referred to as “palpitations”
Clinically these uncoordinated contractions are known as arrhythmias, a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart

Varied causes, classification by:

rate (normal, tachycardia, bradycardia)
mechanism (automaticity, re-entry, fibrillation)
site of origin (e.g., atrial or supraventricular)

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6
Q

What are the three types of arrhythmias?

A

Atrial fibrillation -very rapid, irregular twitching in the atrium, when the ventricular heart rate is not too fast

Atrial flutter - rapid but regular contractions in the atrium, when the ventricular heart rate is not too fast

Ventricular fibrillation - uncoordinated contraction of the cardiac muscle of the ventricles in the heart. As a result, the heart fails to adequately pump blood; hypoxia soon occurs, followed by unconsciousness within twenty to thirty seconds.

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7
Q

What are the signs and symptoms of arrhythmias?

A

Palpitations - described by patients as pounding, or fluttering sensations felt in the chest or neck
skipping beats - changes in the pattern of the pulse
Fainting, light-headedness, dizziness
Chest pain
Shortness of breath (dyspnoea)
Paleness
Sweating
Cardiac arrest
ALWAYS REMEMBER that the patient may not have symptoms!

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8
Q

What are the causes of arrhythmias?

A
Causes can be benign, such as:
Caffeine, exercise or stress
idiopathic or physiological
hyperthyroidism drug side effect
Causes can also be serious:
Coronary artery disease
Cardiomyopathy
Complete heart block
Aneurysm
Valvular disease
Immediate referral is indicated in prolonged palpitations, family Hx of sudden death of cardiac origin, or existing cardiac pathology
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9
Q

What is heart failure?

A

Congestive heart failure (CHF), congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood through the body

Heart muscle disease
Ischaemic heart disease, cardiomyopathy
Restricted filling
Constrictive pericarditis, tamponade, restrictive cardiomyopathy
Inadequate heart rate
Heart block, post infarction, β-blockers
Effect of drugs that alter the force of contraction (inotropes) – Ca channel blockers
Chronic excessive after load - aortic valve stenosis or hypertension

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10
Q

What is left sided heart failure?

A

The left side of the heart pumps blood from the lungs to the organs
L side failure/congestion of the pulmonary vasculature (veins) and symptoms that reflect this AND reduced supply of blood to the tissues
Dyspnoea, possibly at rest; tachypnoea
Easy fatigueability
Orthopnea - increasing breathlessness on reclining, often measured in the number of pillows required to lie comfortably
Paroxysmal nocturnal dyspnea - a night time attack of severe breathlessness, usually several hours after going to sleep
Poor circulation to the body leads to dizziness, confusion and diaphoresis and cool extremities at rest; cyanosis

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11
Q

What is right sided heart failure?

A

The right side of the heart pumps blood returned from the tissues to the lungs to exchange CO2 for O2.
R side failure: congestion of peripheral tissues
This may lead to:
increased jugular venous pressure
peripheral edema or anasarca and nocturia (frequent nighttime urination when the fluid from the legs is returned to the bloodstream).
in more severe cases, ascites (fluid accumulation in the abdominal cavity) and hepatomegaly (painful enlargement of the liver) may develop
Right-side failure – cor pulmonale is due to chronic pulmonary hypertension – oedema secondary to pulmonary disease, pulmonary vascular disorders

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12
Q

What are signs of heart failure?

A

General signs indicating heart failure are a laterally displaced apex beat (as the heart is enlarged) and a gallop rhythm

Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

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13
Q

What is valve disease caused by?

A

Disease, e.g., calcification, RA, SLE
Congenital deformity
Infection e.g., rheumatic fever

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14
Q

What are the 3 types of valve deformity classifications?

A

3 types of valve deformity classifications

Stenosis - narrowing
Insufficiency – doesn’t close properly
Prolapse

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15
Q

What are the two main problems in heart and valve failure?

A

Valves that don’t shut properly, causing regurgitation of blood back across the valve in the wrong direction (for example, from the aorta back into the heart)

Valves that won’t open properly, known as stenosis of the valve, which means blood flow through the valve is limited. For example a condition known as called mitral valve prolapse, or floppy valve syndrome.

One of the cusps on the valve flips back the wrong way, making a characteristic clicking sound and a murmur. It’s now thought that as many as two per cent of adults have this syndrome and is considered a variation of normal and not a disease at all.

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16
Q

What is mitral valve failure?

A

10% of population have a variation in the connective tissue of the mitral valve leaflets that predisposes to prolapse
This protrusion of the leaflet can be heard as a click during ventricular systole
A murmur, produced when blood regurgitates back through the valve may also be present – effectively pressurises the pulmonary circuit
Frequently associated with an ANS imbalance, called dysautonomia
Thus linked with other conditions like Fibromyalgia
Symptoms of fatigue, shortness of breath, palpitations, chest pain, mild depression, anxiety, panic attacks and also, Migraine

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17
Q

What is hole in the heart?

A

About 1 in 100 people have a congenital heart defect
Defects include septal defects, shunts between the great vessels and congential stenosis of pulmonary, aortic or tricuspid valves
Usually require surgical correction
Undiagnosed they form the most common cause of sudden death during sport
Often can place the heart under long term stress, triggering other problems and adaptations

An atrial septal defect (ASD) is a hole in the heart between the upper chambers (atria). The hole increases the amount of blood that flows through the lungs. The condition is present at birth (congenital heart defect). Small atrial septal defects might be found by chance and never cause a concern.

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18
Q

What is hypertrophic cardiomyopathy?

A

Sudden Death Syndrome - unexpected and unexplained death occurring in apparently healthy young people e.g., while on rugby field or football field (Fabrice Muamba)

diagnosis by family history of sudden death
muscle becomes excessively thick and the fibres are arranged haphazardly making the heart vulnerable to some dangerous and potentially fatal heart rhythms (ventricular fibrillation / ventricular tachycardia).

In 25% there is left ventricle outlet obstruction from asymmetrical septal hypertrophy

Autosomal dominant inheritance

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19
Q

What is coronary artery disease?

A

The heart pumps blood to itself first directly at the junction of the aorta

The resting heart extracts 75% of the oxygen so the only way to increase supply is to increase flow

This is achieved by adenosine that is released as the oxygen content of the blood falls and adrenaline and noradrenalin

All of these factors dilate the coronary arteries

reduced pumping occurs if the oxygen supply is restricted (although myoglobin does provide a limited source of oxygen)

CAD is a condition in which plaque builds up inside the coronary arteries, causing a narrowing of the lumen.

Increased likelihood that blood clots (thrombus formation) will form in arteries, partially or completely blocking blood flow

Thrombus can break free forming an Embolus

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20
Q

What are signs and symptoms of coronary artery disease?

A

Signs & Symptoms

Angina

Referred pain
What is the mechanism?

Heart attack/myocardial infarction (MI)

blood flow to an area of heart muscle is completely blocked causing cell death, permanent impairment or death.
What would be the complications of a heart attack if the patient survives?

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21
Q

What are the two types of angina?

A

Angina

The main symptom of angina is a dull, heavy or tight pain in the chest that can sometimes spread to the left arm, neck, jaw or back. The pain is usually triggered by physical activity or stress and usually only lasts for a few minutes.

Two types occur;

Stable – where symptoms develop gradually over time and appear at times of stress/load. They quickly disappear especially with GTN spray

Unstable – Symptoms develop rapidly and persist, often resistant to GTN. A medical emergency

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22
Q

What is atherosclerosis?

A

Atherosclerosis (Atheroma)

Athera meaning porridge
the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques

Disease of the large and medium sized arteries characterized by fibrosis, lipid deposition and chronic inflammatory response

Atheroma, when combined with hypertension can cause aneurisms, which can then burst, causing a bleed. This is a major cause of strokes.

Risk factors: smoking, obesity, dietary, hypertension, low socio-economic status

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23
Q

What is arteriosclerosis?

A

Arteriosclerosis

Arterio meaning artery
Age related changes to the muscular vessel wall
Loss of strength and elasticity (hardening of artery)
Evident after 40
Physiological changes in the intima, replacement of the muscle and elastin with collagen

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24
Q

Where does atherosclerosis usually occur?

A

Affects medium and large arteries especially of heart, brain and kidneys

Plaques often occur in:

areas of turbulent flow particularly in hypertension e.g., branch points
situations where there is a continuous inflammatory stress as a result of chemical abnormalities or some infections

Is the leading cause of death in the developed countries (2 x cancer)

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25
Q

How does an atheroma develop?

A

Development of an atheroma

Damage to the endothelium causes an inflammatory response
Monocytes and T cells are activated and move through the endothelium to the artery’s wall
Monocytes/MΦ collect fatty materials, mainly cholesterol and become foam cells
Smooth muscle cells move from the middle layer into the lining of the artery’s wall and proliferate.
Connective and elastic tissue materials also accumulate there, as may cell debris, cholesterol crystals, and calcium
This accumulation of fat-laden cells, smooth muscle cells, and other materials forms a patchy deposit called an atheroma or atherosclerotic plaque.
The plaque grows narrowing the vessel 🢡🠟 blood flow
Plaques may rupture initiating local clotting that may block the artery or the thrombus may break off and embolise

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26
Q

How is arteriosclerosis different than atheromas?

A

It is generalised and doesn’t come in localised plaques.
It affects both the tunica media and intima.
It is not due to fat.
It does not often cause ischaemia – there is only slight narrowing.
When it is due to hypertension it affects arterioles more than arteries and particularly damages the kidney.

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27
Q

What are aneurysms?

A

Defined as a pathologic dilatation of a segment of a blood vessel
May involve all three layers – ‘true’ or the two inner layers – ‘pseudoaneurysm’

Several types:
fusiform – affects whole circumference
saccular/‘berry’ – bubble-like outpouching – typically found in brain
dissecting – hemorrhage into tunica media separates the layers

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28
Q

What are signs and symptoms of aneurysms?

A
Tenderness or pain in the chest
Back pain (Character?)
Hoarseness & Cough
Shortness of breath
Pulsatile distension of abdomen
 Often asymptomatic until ruptured
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29
Q

What are the signs and symptoms of an abdominal aortic aneurysm?

A

Abdominal Aortic Aneurysm (AAA)

typically men, >50 years old; (50% of AAA’ers are hypertensive)
SOB on exertion
deep penetrating pain in the back or the side of the abdomen
steady gnawing pain in the abdomen that lasts for hours or days at a time
pulsatile mass in the abdomen
possibly detectable by palpation and/or bruits
claudication; coldness, numbness, or tingling in feet due to disturbed blood flow to LEx – possibly intermittent
if an AAA ruptures it is frequently FATAL. Symptoms can include sudden, severe pain in the lower abdomen and back; nausea and vomiting; clammy, sweaty skin; lightheadedness; and a rapid heart rate when standing up
internal bleeding from a ruptured AAA can cause physiological shock due to hypotension

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30
Q

Where is a common site of brain aneurysms?

A

Circle of Willis

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31
Q

What is Reynaud’s phenomenon?

A

Raynaud’s disease is a common condition that affects the blood supply to certain parts of the body, usually the fingers and toes.

blood vessels go into a temporary spasm which blocks the flow of blood. This causes the affected area to change colour to white, then blue and then finally red as the blood flow returns.

Raynaud’s is usually triggered by cold temperatures or by anxiety or stress.

There are two types of Raynaud’s. :

primary: when the condition develops by itself (this is the most common type)
secondary: when it develops in association with another health condition

The causes of primary Raynaud’s are unclear. However 1 in 10 people with primary Raynaud’s will go on to develop a condition associated with secondary Raynaud’s such as lupus or RA.

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32
Q

What happens during a stroke?

A

When the supply of blood is interrupted the brain cells are damaged or killed

Sufferers may become numb, weak or paralysed on one side of the body. They may slur their speech and find it difficult to find words or understand speech. Some people lose their sight or have blurred vision, and others become confused or unsteady.

In virtually all cases a stroke attack does not present with a headache

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33
Q

What is peripheral artery disease?

A

Disease of the distal arteries and arterioles
Usually affects the iliac vessels or more distal
Almost always associated with CHD/CAD via atherosclerosis
May be chronic or acute

Risk factors;

smoking
diabetes
abnormal lipid profile; hyperlipidemia/cholesterolaemia
hypertension
hyperhomocysteinaemia
renal/heart disease (family history)
high levels of fibrinogen
age and gender; 7% middle-aged men; 4% women; 2/1000/yr at 30yrs; 6/1000/yr at 60; 7/1000/yr at 70yr
ethnicity; caucasians >indo-asians & afro-Caribbeans

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34
Q

Signs and symptoms of chronic peripheral artery disease?

A

intermittent claudication (limping) – brought on by exercise, often worse going uphill, affects calf more often than buttock/thighs
Cold extremities (usually LEx)
Changes to skin (dry) and nail quality, loss of hair (‘trophic changes’)
Pain, severe/unremitting (in foot) at rest that disturbs sleep – may be helped by dangling foot over edge
Ulcers/gangrene
Absent/weak/delayed pulses e.g., radiofemoral delay (uni-/bi-?)
Bruit at site of stenosis
Pallor on elevation

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35
Q

Signs and symptoms of acute peripheral artery disease?

A

Symptoms; the 5 P’s

pain
pallor
parasthesia
paralysis
perishly cold extremities

Signs

🡻 pulses
cold marbled/mottled skin
🡻 sensation and motor
may have compartment syndrome e.g., in calf

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36
Q

What are varicose veins?

A

The veins and/or their semilunar valves are stretched and less/ineffective in assisting venous return
May also form “spider veins” under the skin; hemorrhoids in rectum; oesophageal varicies in alcoholics
Varicose veins usually lead to phlebitis and subsequent thrombosis

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37
Q

What are features and risks of varicose veins?

A

Features

Poor appearance of the legs
Pain: aching, throbbing, tingling, sharp
Cramps, heaviness, tiredness of legs
Restless” legs at night
itching, dermatitis, hyperpigmentation, ulceration of the skin, bleeding, blood clots

Risks

Family history (80% M+F; 50% one; 20% neither)
Pregnancy
Sedentary lifestyle - less venous return by the muscular pump. Sitting cross-legged!
Exacerbated by standing for long periods, or other activities which allow the blood to pool due to inertia
Damage due to previous clotting episodes
Obesity

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38
Q

What is superficial thrombophlebitis?

A

Superficial Thrombophlebitis

Often a consequence of varicose veins
Vein wall becomes inflamed leading to thrombus formation
Painful, tender, cord-like structures, redness and swelling
Usually responds to NSAID’s
Embolism not a problem

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39
Q

What occurs in a DVT?

A

Unlike superficial thrombophlebitis the thrombus forms in the vein
Often in the calf, frequently following MI or in 50% of prostatectomy patients
Axillary DVT may occur following trauma
Often associated with pulmonary embolism but this is mainly from iliofemoral DVT

Clot usually initiates around valves of deep veins and is composed of RBC’s and fibrin
Is more likely to occur if blood flow is slow (e.g., in reflux
It propagates as a thrombus of platelets and fibrin and is more likely to embolise

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40
Q

What are the risk factors and signs & symptoms of DVT?

A

Risk factors

Varicose veins
Obesity, stasis, especially inactivity (long flights/bed rest)
Pregnancy
Disorders of clotting & Thrombocythaemia
MI
Surgery

Signs & Symptoms

Pain in the calf with swelling & redness
Engorged superficial veins
Affected limb warmer
Sometimes ankle oedema
Iliofemoral DVT present with severe pain but few other signs!
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41
Q

What is erythropoiesis?

A

Erythropoiesis is stimulated by hypoxia (lack of oxygen) which stimulates the production of a hormone, erythropoietin.

Erythropoietin is a glycoprotein formed within the kidney. It is inactivated by the liver and excreted in the urine

Various other factors can affect the rate of erythropoiesis by influencing erythropoietin production.

Thyroid hormones, thyroid-stimulating hormone, adrenal cortical steroids, adrenocorticotrophic hormone, and human growth hormone (HGH) all promote erythropoietin formation and so enhance red blood cell formation (erythropoiesis

However, very high doses of steroid hormones seem to inhibit erythropoiesis.

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42
Q

What are the signs and symptoms of anaemia?

A
Fatigue
Dyspnoea
Palpitations
Headache
Tinnitus
Anorexia
Dyspepsia
Bowel disturbance
Angina (if CHD)
Low [Hb]
Abnormal MCV
Abnormal TIBC
Pallor
Tachycardia
Murmur
Cardiac enlargement
(Heart failure)
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43
Q

How is anaemia defined?

A

Anaemia is the commonest form of blood disorder.

It is defined as a lack of haemoglobin rather than a reduction in red blood cells

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44
Q

What are the three types of anaemia?

A

Hypochromic, normochromic, hyperchromic

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45
Q

What is the most common type of anaemia?

A

The most common form of anaemia (about 30% of the world population) is hypocytic hypochromic anaemia.

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46
Q

When is normocytic anaemia seen?

A

In the UK we often see normocytic anaemia where the erythrocytes are averaged sized but low in numbers within the formed blood.

Typically this will be as a result of;

Chronic Disease
Kidney Disease
Pregnancy
Bone Marrow Failure

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47
Q

How does macrocytic anaemia present?

A

The other commonly observed form of anaemia is macrocytic which can present;

Where large immature dysfunctional erythrocytes are present in bone marrow due to defective DNA synthesis (Megaloblastic)

Less common is Non-megaloblastic anaemia which is usually caused by alcohol abuse. DNA synthesis is not defective, and there are no megaloblastic changes in the bone marrow

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48
Q

What is megaloblastic anaemia?

A

Megaloblastic anemia is a condition in which the bone marrow produces unusually large, structurally abnormal, immature red blood cells (megaloblasts). Bone marrow, the soft spongy material found inside certain bones, produces the main blood cells of the body -red cells, white cells, and platelets.

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49
Q

What are the causes of anaemia?

A

Blood loss e.g. Trauma

Decreased production e.g. Iron deficiency

Increased destruction e.g. Sickle Cell

Sequestration e.g. Polycythaemia

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50
Q

What is pernicious anaemia?

A

Commonly caused by loss of gastric parietal cells, and subsequent inability to absorb vitamin B12. May also be linked to other reasons for malabsorbtion e.g. Crohn’s disease or inflammatory conditions of the small intestine.

Can also be due to dietary insufficiency – common in vegetarians and vegans

May be due to increased requirement, such as in pregnancy or where cancers may be widespread in tissue

Less commonly due to parasitic competitive upteake e.g fish tapeworm

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51
Q

What are signs and symptoms of sickle cell anaemia?

A

Episodes of pain during a sickle cell crisis are one of the most common symptoms

A sickle cell crisis is triggered when the abnormal blood cells block the small blood vessels that supply the body’s tissue.

As a child grows older, pain can affect any area of the body, although the most common areas are:
ribs 
spine 
pelvis 
abdomen 
sternum (breastbone) 
long bones in the legs and arms
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52
Q

What is sequestration in anaemia?

A

Erythrocytes become entraped within organs or other tissue – commonly in an enlarged spleen (Felty’s Syndrome)

Splenomegaly results from the chronic inflammatory state.
The increased miles of sinusoids in this massive spleen leads to;

Shortened RBC life span (extravascular haemolysis)
Thromobytopaenia (easy of bruising) and
Leukopaenia, which leads to chronic bacterial infections

Often aggrivated by a dilutional anaemia due to increased plasma volume.

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53
Q

What is polycythaemia?

A

A range of disorders which have an increased number of circulating erythrocytes

The normal Hematocrit (packed cell volume – PCV) is 52% for males and 47% for females.

Two forms;

Relative Polycythaemia where there is a decrease in plasma volume
Absolute Polycythaemia where there is an increase in erythrocyte numbers
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54
Q

What is haemochromatosis?

A

A recessive genetic disorder causing the body to absorb an excessive amount of iron from the diet

The iron is then deposited in various organs, mainly the liver, but also the pancreas, heart, endocrine glands, and joints

Once believed to be rare, but now accepted as one of the most common genetic disorders

Blood tests identify the condition which is treated by weekly removal of blood.

Significant for osteopaths as arthritic symptoms are part of the common and earliest presentation

55
Q

What are signs and symptoms of haemochromatosis?

A

Chronic fatigue, weakness, lethargy
Abdominal pain; sometimes in the stomach region or the upper right hand side, sometimes diffuse
Arthritis; may affect any joint but particularly common in the knuckle and first joint of the first two fingers (the bronze fist - illustrated on the right)
Diabetes (late onset type)
Liver disorders; abnormal liver function tests, enlarged liver, cirrhosis
Sexual disorders; loss of sex drive, impotence in men, absent or scanty menstrual periods and early menopause in women, decrease in body hair
Cardiomyopathy; disease of the heart muscle (not to be confused with disease of the arteries of the heart)
Neurological/psychiatric disorders; impaired memory, mood swings, irritability, depression
Bronzing of the skin, or a permanent tan

56
Q

What is leukaemia?

A

Neoplasia of white blood cell precursors within lymphoid (lymphatic) or myeloid (bone marrow) tissues

Classified as acute or chronic, where acute conditions tend to be curable if treated early, whereas chronic conditions are much more difficult to treat

57
Q

What is the aetiology of acute leukaemia?

A

ALL; Infants 2-4 years old most at risk, but can occur in later life. 2/3 of children cured upto the age of 5, decreasing success in later life.

AML; More common in later life though infants and adolescents can develop it. Only 25% of sufferers live for longer than 5 years.

Treated with chemotherapy and antibiotics, plus blood replacements with the aim of eliminating the abnormal tissue and allowing it to repopulate. Bone marrow transplants commonly carried out.

58
Q

What are signs and symptoms of acute leukaemia?

A

Aches & pains (hence the visit to an osteopath)
Bone pain (especially in children – hence the visit to the osteopath
Non-specific flu like symptoms
Fever, malaise
Anaemia
Bleeding gums, noses and purpura present
Infections of bacteria and fungi due to neutropenia
Headaches, fits, convulsions and comas (due to increased blood viscosity)
Enlargement of lymph nodes, liver and spleen

59
Q

What is chronic leukaemia?

A

CLL; Commonest type of leukaemia in the UK (30% of presentations) affects mature lymphocytes only.

CML; Several cell types involved (myeloproliferative) accounts for 15-20% of lymphomas.

60
Q

What are signs and symptoms of chronic leukaemia?

A

Lethargy & fatigue
Splenomegaly – in severe cases the spleen fills the abdominal and pelvic cavities
Moderate anaemia
Hepatomegaly
Friction rub and tender abdomen common (hence visit to osteopath)
Enlarged lymph nodes

61
Q

What is myeloma?

A

Often known as multiple myeloma

Neoplasm affecting plasma cells which arise in bone marrow and causing a breakdown in the production of antibodies.

Commoner in males than females, incidence is increasing due to better detection

Common in elderly (over 75) with higher incidence in Afro-Caribbean origin

Causes bone marrow failure, as well as bone destruction which means sufferers are contra-indicated for HVT

62
Q

What are signs and symptoms of myeloma?

A

Bone pain or insidious fractures due to resorbtion (may visit an osteopath)
Red Blood Cells aggregation due to increased paraprotein in blood
Kidney damage due to an increase in calcium deposition and effects of the paraprotein.

63
Q

What is lymphoma?

A

Neoplasm of lymphoid cells, principally affecting the lymph nodes (neoplastic lymphadenopathy)

Two main categories;

Hodgkin’s Lymphomas (Hodgkin’s Disease)
Non-Hodgkin’s Lymphomas

64
Q

What is Hodgkins lymphoma?

A

Syndrome rather than a single disease typified by characteristic malignant cells (Reed-Sternberg Cells)

1% of malignant diseases, with male to female ratio of 1.5:1

Bimodal age distribution with peaks at 20-30 and over 65

Possible links with the Epstein-Barr Virus (EBV) and reported association with HIV

Treated with chemotherapy & radiotherapy with hypothyroidism a common complication. 75% survival rate after 5 years. Fatal if not treated

65
Q

What are signs and symptoms of Hodgkins Lymphoma?

A

Painless enlarged lymph nodes which are firm, rubbery and mobile.
Can be mediastinal and affect breathing
Weight loss & night sweats with flu-like symptoms
Pruritis common

66
Q

What is non-Hodgkins lymphoma?

A

A more prevalent condition than Hodgkin’s Lymphomas accounting for 3% of all malignancies.

Complex scheme of classification but the most common affects the older age group and is known as Follicular Lymphoma

Similar signs & symptoms to Hodgkin’s Lymphomas but extranodal involvement is more likely, with the lymphomas being more widespread than the patient is aware.

Radiotherapy, chemotherapy and bone marrow suppression with stem cell transplants may be used in treatment. Breakdown of tumours may lead to cardiac arrest due to release of high levels of potassium

67
Q

What are the most common sites of haemorrhage?

A

Commonest sites of blood loss are;

Uterine – menstrual loss especially in the case of menorrhagia
Gastric/Gut – peptic ulcers, haemorrhoids, NSAIDS, neoplastic disease.

Also;

In Urine, haematuria due to damaged glomeruli
Internally from damaged blood vessels (risk of septacaemia)
From capilliaries resulting in small petechial haemorrhages

68
Q

What are three types of skin haemorrhages?

A

Purpura are a collection of petechial haemorrhages in the skin and mucus membranes e.g. Senile purpura

Ecchymosis (bruise) is a large, subcutaneous haemorrhage

Haematoma is a large haemorrhage – a lump of clotted blood

69
Q

What is haemophilia?

A

Two types, both are sex-linked recessive disorders

 Haemophilia A (Classical)
 Haemophilia B (Christmas Disease)

Specific clotting factors are absent

Males affected and females carriers, but with 50% deficiency in clotting factor therefore a mild form may be present.

Severity varies between families

No purpura but frequent haemorrhaging into large joints (haemarthrosis) resulting in synovial hypertrophy, erosion of articular cartilage and severe osteoarthritis.

Bleeding into muscle and urinary tract may also occur

70
Q

What are some general red flags?

A

Unexplained weight loss
Fever of unknown origin, especially if prolonged or recurring, or occurring as night sweats
* Diastolic blood pressure > 140 mmHg. Or a systolic pressure of < 80 mmHg.
Symptoms or signs of psychosis or self harm.
Enlarged generalised lymph nodes or enlarged, matted, fixed or irregular lymph nodes.
* Symptoms and signs of any notifiable diseases (Public Health control of disease act 1984)

71
Q

What are some head red flags?

A

Persistent, unremitting head pain with or without visual disturbance. May be worse at night or wake patient from sleep.
* Sudden onset severe headache, with or without brief syncope, followed by vomiting , dizziness and possible neck stiffness.
* Sudden, severe headache with weakness on one side of mouth and face, unequal pupils, arm weakness and pronator drift, confused or emotional state
Visual disturbances, vertigo, syncope and loss of conciousness

72
Q

What are some neck red flags?

A

sore throat, fever, neck rigidity, Kernig’s sign, Brudzinski’s sign, later purpural rash.
* Sudden onset sore throat with hoarseness and high fever, developing into dyspnoea, dysphagia, drooling and inspiratory stridor.

73
Q

What are some chest red flags?

A
  • Unidentified chest pain, crushing or vice-like, pain possibly referring to jaw, shoulder or arm especially on left side, pain unrelieved by rest or angina medication.
  • Grossly elevated venous pressure with raised JVP, possibly with dyspnoea, oedema, frothy possibly bloodstained sputum.
  • Sudden onset excruciating pain in praecordium or interscapular area may be described as “tearing” or “ripping”
    Persistent cough lasting more than 3-4 weeks especially when associated with night sweats, weight loss, malaise, or if unexplained.
  • Fever and cough, possibly preceded by upper respiratory infection. Sudden chill followed by high fever, rapid pulse and breathing rate, chest pain on involved side , dyspnoea with purulent, blood streaked or rusty coloured sputum.
    Persistent monophonic wheeze.
    Blood in sputum.
    All undiagnosed breast lumps, skin changes or discharge from nipples
74
Q

What are some abdomen red flags?

A

Widened aortic pulse in abdomen
Haematemesis – frank red, brown or “coffee grounds”
* Persistent or severe vomiting
* Absence of bowel sounds or high pitched bowel sounds, possibly accompanied by pain, rebound tenderness, distension, obstipation and vomiting
Melaena stools (altered black, tarry blood) or unexplained frank blood on stool
Jaundice
Ascites
Dysphagia
Unexplained changes in bowel habit
Haematuria, proteinuria, glucosuria
Vaginal bleeding > 6months after menopause or any time during pregnancy, or unexplained menorrhagia or metrorrhagia.

75
Q

What are some lower limb red flags?

A
  • Soreness in calf on walking relieved by rest or elevation with deep calf tenderness on examination
  • Acutely inflamed single joint, pain with heat and swelling, particularly involving the knee, with possible history of recent infection, RA, or chronic arthritis.
    Persistent progressive pain especially associated with a mass.
    Unexplained bone pain or spontaneous fractures
    Pain in joint accompanied by dislocation, subluxation, effusion (possibly haemorrhagic) with history of diabetes, alcoholism or degenerative spinal lesions
    Bilateral radicular leg symptoms with possible impaired sphincter and sexual function
    Persistant unexplained paresthesia or numbness possibly accompanied by muscle weakness or wasting.
76
Q

What are some skin red flags?

A

local or systemic fever and malaise
tracking from one group of swollen lymph nodes to next – red line
* psoriasis becoming pustular, erythematous and generalised
* signs of swelling and peau d’orange skin or well defined red swollen border and central blistering
* generalised red scaly skin – exfoliating dermatitis
ulcerative lesion which will not heal
changes in mole size >6mm diameter and or colour
unilateral eczematous rash around nipple
multiple blisters erosions or ulcers involving the mouth and lips associated with target lesions
ABCDE – Asymmetry, Border irregularity, Colour irregularity, Diameter >6mm, Elevation and enlargement.

77
Q

When should abdominal pain be refered?

A
A raised temperature. 
The passage of blood per rectum (red or black) or hematemesis. 
Persistent vomiting. 
Dark or bright red vaginal bleeding. 
Pain: 
– which lasts for more than 4 hours
– with diarrhoea which lasts for more than 24 hours
– which is severe, localized, and related to meals
– which disturbs sleep
– with faintness.
Chronic or recurrent abdominal pain associated with one or more of the following: 
anaemia
– significant weight loss
– chronic diarrhoea
– nocturnal diarrhoea or pain
– chronic constipation
– steatorrhoea.
78
Q

When should polyarthritis be referred?

A
– weight loss
– fever
– lymphadenopathy
– extensive rash
– symptoms in more than one system
– vasculitis
– heart murmurs
– severe pain/disability
– extreme fatigue
– increasing severe/intractable joint pain.
79
Q

Skin disease can be classified as:

A

Skin diseases can be classified as:
Non-infectious
Infectious
Malignant

80
Q

Describe the benefits of viewing the skin with a dermoscope or Wood’s light.

A

Dermascope enables deeper structures to be seen, without any interference by reflection and refraction of light in the epidermis

Wood’s Light
in hypopigmentation (vitiligo) if helps to determine extent of disease
In pigmented conditions (melasma) can determine if pigmentation is epidermal or epidermal & dermal
Can help to diagnose some fungal infection

81
Q

What is a macule?

A

Flat area of skin ≤ 1cm∅ usually different colour to surrounding skin

82
Q

What is a papule?

A

Same as macule but larger

83
Q

What is a plaque?

A

A raised area of skin with a flat top > 1cm ∅

84
Q

What is a pustule?

A

A visible accumulation of pus in a blister

85
Q

What is a vesicle?

A

A small fluid filled blister ≤ 1cm∅

86
Q

What is a petechiae?

A

Pinhead sized flat macules of extravascular blood in the dermis

87
Q

Describe the relationship between pain and itch and the classification of pruritus?

A

Relationship between pain and itch is inhibitory Scratching either causes inhibition of itch (by stimulating ascending sensory pathways that inhibit itch at the spinal cord) or interferes directly with cutaneous itch fibres by direct damage

Terms itch and pruritis are synonymous however pruritus is often used when itch is generalised. Itch can arise from primary cutaneous disease or from systemic disease, which may cause itch by central or peripheral mechanisms. Even when mechanism is peripheral, there are not always signs of primary skin disease.

88
Q

What is eczema?

A

Eczema or dermatitis describes a skin reaction in which the acute stages there is itching, redness, some swelling, damp oozing from the skin and vesicles. Itching can be so intense as to provoke scratching that leads to bleeding. In more chronic cases dryness and thickening of the skin is more prominent.

Clinical features
Atopic eczema is extremely itch and scratching accounts for many of the signs.
Widespread cutaneous dryness/roughness is another feature.
The distribution and character of rash vary with age.

Red to brownish-gray colored patches
Itching, which may be severe, especially at night
Small, raised bumps, which may leak fluid and crust over when scratched
Thickened, cracked or scaly skin
Raw, sensitive skin from scratching

89
Q

What is atopic eczema?

A

Atopic eczema is generalised prolonged hypersensitivity to common antigens eg house dust mite, pollen

Aetiology.
Genetic factors are important,
Epidermal barrier impairment is a major factor in this type of eczema.
Environmental factors (exposure to allergens in utero or during childhood) may also have role.
60-80% of individuals are genetically susceptible to the induction of IgE (immunoglobin E – antibody produced by immune system) mediated sensitisation to environmental allergens such as food and animal hair.
Decreased skin barrier function may also allow greater penetration of allergens through epidermis thus causing immune stimulation and subsequent inflammation

90
Q

What is seborrheic dermatitis?

A

Atopic eczema is generalised prolonged hypersensitivity to common antigens eg house dust mite, pollen

Aetiology.
Genetic factors are important,
Epidermal barrier impairment is a major factor in this type of eczema.
Environmental factors (exposure to allergens in utero or during childhood) may also have role.
60-80% of individuals are genetically susceptible to the induction of IgE (immunoglobin E – antibody produced by immune system) mediated sensitisation to environmental allergens such as food and animal hair.
Decreased skin barrier function may also allow greater penetration of allergens through epidermis thus causing immune stimulation and subsequent inflammation

91
Q

What is discoid eczema?

A

Common, consists of discrete coin shaped eczematous lesions, often impetiginised and commonly occur on limbs of men

92
Q

What is irritant eczema?

A

Detergents, alkalis, acids solvents and abrasives are common irritants, individual susceptibility varies. Elderly, atopic and fair skinned are predisposed. Accounts for occupational cases and causes time off work

93
Q

What is allergic contact eczema?

A

Due to delayed hypersensitivity reaction following contact with antigens Previous allergen exposure is required for sensitisation and reaction is specific to the allergen or closely related chemicals eg. Nickel (jewellry, bra clips), rubber chemicals (clothing shoes), parabens (cosmetics) etc long long list

94
Q

What is gravitational eczema?

A

Occurs in lower leg, often associated with signs of venous insufficiency, oedema, loss of hair, ulceration

95
Q

What is lichen simplex?

A

Occurs secondary to chronic rubbing and scratching, localised include neck, lower legs and anogenital region

96
Q

What is pompholyx?

A

Intensely itchy vesicles occur on palms, sides of fingers and soles. Causes – atopic eczema, allergic and fungal infection

97
Q

What is psoriasis?

A

Psoriasis is a chronic inflammatory disease of the skin characterised by erythematous plaques with silvery scales which occurs on extensor surfaces and scalp.

It can start at any age including childhood, with peaks of onset at 15–25 years and 50–60 years. It tends to persist lifelong, fluctuating in extent and severity. It is particularly common in Caucasians but may affect people of any race.

Psoriasis is multifactorial. It is classified as an immune-mediated inflammatory disease (IMID).
Psoriasis usually presents with symmetrically distributed, red, scaly plaques with well-defined edges. The scale is typically silvery white, except in skin folds where the plaques often appear shiny and they may have a moist peeling surface. The most common sites are scalp, elbows and knees, but any part of the skin can be involved. The plaques are usually very persistent without treatment.
Itch is mostly mild but may be severe in some patients, leading to scratching and lichenification (thickened leathery skin with increased skin markings). Painful skin cracks or fissures may occur

98
Q

What are the different types of psoriasis?

A

Plaque psoriasis. Most common form. Sites include extensor surfaces – elbows knees, and lower back. Other sites – scalp, nails, palms

Guttate psoriasis. Most common in kids and adolescents, may present after streptococcal throat infection. Individual lesions droplet shaped, small less than 1cm, erythematous, scaly and numerous

Erythrodermic psoriasis
Generalised erythrodermic psoriasis is a medical emergency

Pustular psoriasis. Generalised or localised. Not common. Patient usually febrile and unwell, this is a medical emergency

99
Q

List 3 key differentiating factors between eczema and psoriasis.

A

SKIN Eczema is red, dry, flaky Psoriasis is dry, scaly with silvery hue & thicker skin

AGE Eczema common in babies & children Psoriasis develops later 15-35yrs

SITE Eczema develops in folds, joints Psoriasis found all over

100
Q

What is acne vulgaris?

A

Acne vulgaris
Acne is almost ubiquitous in the teenage years and results from an increase in androgen production which increases sebum excretion. The excessive sebum leads to blockage in the sebaceous ducts and infection with Propionibacterium acnes.

101
Q

Describe the clinical features of acne vulgaris.

A

Usually affects face and often the trunk
Greasiness of the skin may be obvious
Individual lesions are centred on the pilosebaceous unit, ie the hair follicle and its associated oil gland.
Several types of acne spots occur, often at the same time. They may be inflamed papules, pustules and nodules; or non-inflamed comedones and pseudocysts.
Scarring may be deep seated or superficial

102
Q

What is acne rosacea?

A

Rosacea usually appears in middle age and is more common in women than men. The initial symptoms are that the cheeks, forehead and nose tend to flush, a feature which is more prominent after alcohol consumption or exposure to the sun. In long standing cases broken veins can appear and pustules develop.

103
Q
Explain how you would distinguish rosacea from:
Acne
Seborrheic dermatitis
Photosensitivity
Systemic Lupus Erythematosus
A

Acne In rosacea, sebum excretion is normal and comedones are absent

Seborrhoeic eczema is scaly, but may coexist with rosacea

Photosensitivity likely to affect all of face not just centre like rosacea??

Systemic lupus erythematosus other symptoms would be present?? (eg severe fatigue, joint pain, swelling headaches?)

104
Q

What is erythroderma?

A

Erythroderma is a generalised condition in which the whole skin surface is inflamed. It results most commonly from an extreme allergic reaction to a medication or from severe extensive eczema or psoriasis. It is a medical emergency as whole skin surface inflammation causes lose of heat and water retention making a patient vulnerable to dehydration, heart and kidney failure, and hypothermia.

105
Q

What is urticaria?

A

Urticaria is an allergic skin reaction with the rapid formation of wheals (area of raised skin) as a result of rapid dilation of dermal blood vessels which allows fluid to pass into surrounding skin tissue. Common allergens include skin contact with plants or animal fur, ingestion of certain foods (eg milk, shellfish, egg, nuts) or response to drugs (eg penicillin).

106
Q

What is lichen planus?

A

Lichen planus is an immune-related skin reaction of unknown cause in which the skin erupts with numerous itchy, purplish, flat-topped papules. The papules most commonly appear on the wrists, ankles and small of the back.

107
Q

What is Pityriasis rosea?

A

Pityriasis rosea
This is a self-limiting condition that primarily affects children and young adults. It may be a delayed response to a viral infection. The rash begins with a so called ‘herald patch’ of red, scaly skin on the trunk or upper arm. Then within a few days there is an eruption of small, pink, oval patches on the back, abdomen, upper arms and thighs.

108
Q

What is impetigo?

A

Impetigo is a common and highly contagious superficial bacterial skin infection. There are two main presenta- tions: bullous impetigo, caused by a staphylococcal epi- dermolytic toxin, and non-bullous impetigo (Fig. 28.17), which can be caused by either Staphylococcus aureus or streptococcus, or both together. Staphylococcus is the most common agent in temperate climates, whereas streptococcal impetigo is more often seen in hot, humid areas. All ages can contract the infection but non-bullous disease particularly affects young children, often in late summer. It can be sporadic, although outbreaks can arise in conditions of overcrowding and poor hygiene or in institutions. A widespread form can occur in neonates. Predisposing factors are minor skin abrasions and the existence of other skin conditions, such as infestations or eczema.

In non-bullous impetigo, a thin-walled vesicle devel- ops; it rapidly ruptures and is rarely seen intact. Dried exudate, forming golden crusting, arises on an ery- thematous base. In bullous disease, the toxins cleave desmoglein-1, causing a superficial epidermal split and the occurrence of intact blisters with clear to cloudy fluid, which last for 2–3 days. The face, scalp and limbs are commonly affected but other sites can also be involved, particularly if there are predisposing factors such as eczema. Lesions may be single or multiple and coalesce. Constitutional symptoms are uncommon. A bacterial swab should be taken from blister fluid or active lesion before treatment commences. Around one- third of the population are nasal carriers of Staphylococ- cus, so swabs from the nostrils should also be obtained.

In mild, localised disease, topical treatment with mupirocin or fusidic acid usually suffices and limits the spread of infection. The use of topical antiseptics and soap and water to remove infected crusts is also helpful. Staphylococcal carriage should be treated, with mupi- rocin topically to the nostrils if swabs are positive. In severe cases, an oral antibiotic, such as flucloxacillin or erythromycin, is indicated. If a nephritogenic streptococ- cus is suspected, then systemic antibiotics should be given, as post-streptococcal glomerulonephritis can occur (p. 498). Underlying disease, such as infestations, must be treated and cross-infection minimised. Scarring does not occur but there may be temporary dyspigmentation

109
Q

What is folliculitis?

A

Hair follicle inflammation can be superficial, involving just the ostium of the follicle (folliculitis) or deep (furun- cles and carbuncles).
Superficial folliculitis
This is very common, usually minor and subacute or chronic. Primary lesions are follicular pustules and ery- thema. It is often infective, caused by Staph. aureus, but can also be sterile and caused by physical (e.g. traumatic epilation) or chemical (e.g. mineral oil) injury. Staphylo- coccal folliculitis is most common in children and often occurs on the scalp or limbs. Pustules usually resolve without scarring in 7–10 days but can become chronic. In older children and adults, they may progress to a deeper form of folliculitis. The condition is often self- limiting and may respond to irritant removal and anti- septics. More severe cases may require topical or systemic antibiotics and treatment of Staph. aureus carrier sites.
Deep folliculitis (furuncles and carbuncles)
A furuncle (boil) is an acute Staph. aureus infection of the hair follicle, usually with necrosis. It is most common in young adults and males. It is usually sporadic but epi- demics occasionally occur. Malnutrition, diabetes and HIV predispose, although most cases arise in healthy subjects. Any body site can be involved but neck, but- tocks and anogenital areas are common. Infection is often associated with chronic Staph. aureus carriage in the nostrils and perineum, and may be due to resistant strains, such as meticillin-resistant organisms (MRSA). Friction caused by tight clothing may be contributory. Initially, an inflammatory follicular nodule develops and becomes pustular, fluctuant and tender. Crops of lesions sometimes occur. There may be fever and mild constitutional upset. Lesions rupture over days to weeks, discharge pus, become necrotic and leave a scar.
If a deep Staph. aureus infection of a group of contigu- ous hair follicles occurs, this is termed a carbuncle and is associated with intense deep inflammation (Fig. 28.19). This usually occurs in middle-aged men, often with pre- disposing conditions such as diabetes or immunosuppression. A carbuncle is an exquisitely tender nodule, usually on the neck, shoulders or hips, associated with severe constitutional symptoms. Discharge, necrosis and scarring are usual.

110
Q

What is a boil or carbuncle?

A

Boils can occur anywhere on your skin, but appear mainly on the face, back of the neck, armpits, thighs and buttocks — hair-bearing areas where you’re most likely to sweat or experience friction. Signs and symptoms of a boil usually include:
A painful, red bump that starts out small and can enlarge to more than 2 inches (5 centimeters)
Reddish or purplish, swollen skin around the bump
An increase in the size of the bump over a few days as it fills with pus
Development of a yellow-white tip that eventually ruptures and allows the pus to drain out
A carbuncle is a cluster of boils that form a connected area of infection. Compared with single boils, carbuncles cause a deeper and more severe infection and are more likely to leave a scar. People who have a carbuncle often feel unwell in general and may experience a fever and chills.

111
Q

What is cellulitis?

A

Cellulitis is inflammation of subcutaneous tissue, due to bacterial infection (Fig. 28.20). In contrast, erysipelas is bacterial infection of the dermis and upper subcutaneous tissue (Fig. 28.21), although in practice it may be difficult to distinguish between them. These conditions are most commonly caused by group A streptococcus. However, culture of swabs from affected sites is often negative. There is frequently a source of organism entry, such as an ear infection, varicose eczema/ulcer or tinea pedis, and swabs should also be taken from these sites. Diabetes and immunosuppression are predisposing factors. The patient usually has malaise, fever and leucocytosis, and streptococcal serology will often be positive. The face (erysipelas) and legs (cellulitis) are most often affected and the site is hot, painful, erythematous and oedema- tous. Blistering often occurs and may be haemorrhagic. Regional lymphadenopathy is common. Erysipelas typi- cally has a well-defined edge due to its more superficial level of involvement, whereas cellulitis is typically ill- defined. Treatment is usually with intravenous anti- streptococcal antibiotics, such as benzylpenicillin, with erythromycin or ciprofloxacin as an alternative for penicillin-allergic patients. Milder cases may be treated with oral antibiotics. If cases are untreated, sequelae include lymphoedema, cavernous sinus thrombosis, sep- ticaemia and glomerulonephritis.

112
Q

What is scalded skin syndrome?

A

Staphylococcal scalded skin syndrome (SSSS) is a poten- tially serious exfoliating condition occurring predomi- nantly in children, particularly neonates. It is caused by systemic circulation of epidermolytic toxins from a Staph. aureus infection. The same toxins are implicated in bullous impetigo, which is a localised form of SSSS. The focus of infection may be minor skin trauma, the umbilicus, urinary tract or nasopharynx. The child presents with fever, irritability and skin tenderness. Erythema usually begins in the groin, axillae and around the mouth. Blisters and superficial erosions develop over 1–2 days and can rapidly involve large areas, with severe systemic upset.

113
Q

What is leprosy?

A

Leprosy, also known as Hansen’s disease, is a chronic, mildly infectious disease caused by slow-growing bacteria called Mycobacterium leprae. Mycobacterium leprae, or M. leprae, multiplies very slowly, with an incubation period of about 3 to 5 years. However, symptoms can take as long as 20 years to appear. It can affect the nerves, eyes, skin, and mucous membranes of the upper respiratory tract.

Leprosy typically appears as patches of discolored skin with a loss of sensation at the affected area. When nerves in the arm are affected, small muscles become paralyzed, leading to curling of the fingers. Patients may also lose sensation in the feet. Unable to feel pain, the patient may suffer deformation of their feet as a result of continued injury and infection. If the facial nerves are affected, they may lose the blinking reflex of the eye, which can lead to dryness, ulceration, and ultimately blindness. Bacilli at the mucous lining of the nose can cause internal damage and scarring which, in time, causes the nose to collapse.

114
Q

What are warts?

A

Papillomaviruses and viral warts
Viral warts are extremely common and are caused by the DNA human papillomavirus (HPV). There are over 90 subtypes, based on DNA sequence analysis, causing different clinical presentations. Transmission is by direct virus contact, in living or shed skin, and is encouraged by trauma and moisture (e.g. swimming pools). Genital warts are spread by sexual activity and show a clear relationship with cervical and intra-epithelial cancers of the genital area.

HPV-16 and 18 appear to inactivate tumour suppressor gene pathways and lead to squamous cell carcinoma of the cervix or intraepithelial carcinoma of the genital skin. Vaccinations are now available against HPV-16 and 18 and are recommended for adolescent females before they become sexually active. The relationship between skin HPV and skin cancer is unclear. Individuals who are systemically immunosuppressed, e.g. after organ transplantation, have greatly increased risks of skin cancer and HPV infection, but a causal link is not certain.

Clinical features
Common warts are initially smooth, skin-coloured papules, which become hyperkeratotic and ‘warty’.
They are most common on the hands but can occur on the face, genitalia and limbs, and are often multiple. Plantar warts (verrucae) have a slightly protruding rough surface and horny rim and are often painful on walking. Paring reveals capillary loops that distinguish plantar warts from corns.
Other varieties of wart include:
• mosaic warts: mosaic-like sheets of warts
• plane warts: smooth, flat-topped papules, usually on the face and backs of hands; they may be pigmented and therefore misdiagnosed
• facial warts: often filiform
• genital warts: may be papillomatous and exuberant.

115
Q

What is chickenpox/shingles?

A

Varicella zoster virus is dermotropic and neurotropic, that produces primary infection and may reactivate later in life. Highly infectious to non-immune individuals. Well tolerated in children, more serious in adulthood, pregnant women and immunocompromised with risk of developing pneumonitis, hepatitis and encephalitis.

Incubation 11-20 days, after which vascular eruptions begin. On mucosa, and on chest. New lesions occur every 2-4 days and associated with fever. Infectivity lasts up to 4 days. Itching may cause secondary bacterial infection.

116
Q

What is molluscum contagiosum?

A

Molluscum contagiosum is caused by a DNA poxvirus skin infection. It is most common in children over the age of 1 year, particularly those with atopic dermatitis. It also frequently occurs in immunosuppressed patients, including those with HIV. Lesions are dome- shaped, ‘umbilicated’, skin-coloured papules with central punctum. They are often multiple and found at sites of apposition, such as the side of the chest and the inner arm. Spontaneous resolution occurs but can take months. Prior to resolution, they often become inflamed and may leave small, atrophic scars. Destructive therapies may be painful and risk scarring, and the decision not to treat is often sensible. Gentle squeezing with forceps after bathing can hasten resolu- tion. Topical salicylic acid, podophyllin, trichloroacetic acid, cryotherapy or curettage is an alternative.

117
Q

What is tinea corporis?

A

Tinea corporis should feature in the differential diagno- sis of a red, scaly rash (p. 1257). Typically, lesions are erythematous, annular and scaly, with well-defined edge and central clearing. There may also be pustules at the active edge. Lesions are usually asymmetrical and may be single or multiple. The degree of inflammation is dependent on the organism involved and the host immune response. Microsporum canis (from dogs) and Trichophyton verrucosum (from cats) are common cul- prits. Ill-advised use of topical steroids can modify the clinical presentation and increase disease extension (tinea incognito).

118
Q

What is tinea cruris?

A

This is extremely common worldwide and is usually caused by Trichophyton rubrum. Itchy, erythematous plaques develop in the groins and extend on to the thighs, with a raised active edge (Fig. 28.24A).

119
Q

What is tinea pedis?

A

This is the most common fungal infection in the UK and USA, and is usually caused by anthropophilic fungi, such as T. rubrum, T. interdigitale and Epidermophyton floccosum. It typically presents as an itchy rash between the toes, with peeling, fissuring and maceration. Involve- ment of one sole or palm (tinea manuum) with fine scaling is characteristic of T. rubrum infection. Vesiculation or blistering is more often seen with T. mentagrophytes.

120
Q

What are scabies?

A

Scabies is caused by the mite, Sarcoptes scabiei. It can lead to secondary infection, sometimes with complications, such as glomerulonephritis due to nephritogenic strep- tococci. It spreads in households and environments where there is intimate personal contact. The diagnosis is made by identifying the scabietic burrow (p. 312 and Fig. 28.25) and visualising the mite (by extracting with a needle or using a dermatoscope). In small children, the palms and soles can be involved, with pustules. Pruritus is prominent. The clinical features include secondary eczematisation elsewhere on the body; the face and scalp are rarely affected, except in infants. Involvement of the genitals in males and of the nipples commonly occurs. Even after successful treatment, itch can continue and occasionally nodular lesions persist.

121
Q

What is head lice?

A

Infestation with the head louse, Pediculus humanus capitis, is common. It is highly contagious and spread by direct head-to-head contact. Scalp itch leads to scratch- ing, secondary infection and cervical lymphadenopathy. The diagnosis is confirmed by identifying the living louse or nymph on the scalp or on a black sheet of paper after careful fine-toothed combing of wet hair following conditioner application. The empty egg cases (‘nits’) are easily seen on the hair shaft (p. 1250) and are hard to dislodge.
Treatment is recommended for the affected individ- ual and any infected household/school contacts. Eradi- cation in school populations is difficult because of poor compliance and treatment resistance.

122
Q

What is basal cell carcinoma?

A

Basal cell carcinoma
The incidence of NMSC has increased dramatically over the last 30 years and basal cell carcinoma (BCC) accounts for more than 70% of cases. In Europe, the ratio of BCC to SCC is 4–5 : 1 in immunocompetent patients. BCC is a malignant tumour that rarely metastasises; it is thought to derive from immature pluripotent epidermal cells and is composed of cells with similarities to basal layer epidermis and appendages. Lesions typically occur at sites of moderate sun exposure, particularly the face, and are slow-growing. Incidence increases with age and males are more commonly affected. Lesions may ulcer- ate and invade locally; hence the term ‘rodent ulcer’. Mutations in the PTCH tumour suppressor gene have been identified and an aberrant hedgehog signalling pathway is implicated in pathogenesis.

Clinical features
Early BCCs usually present as pale, translucent papules or nodules, with overlying superficial telangiectatic vessels (nodular BCC). If untreated, they will increase in size and ulcerate, to form a crater with a rolled, pearled edge and ectatic vessels (Fig. 28.9). There may be some pigmentation or a cystic component. A superficial multi- focal type can occur, often on the trunk, and may be large (up to 10 cm in diameter); there may be multiple lesions. Superficial BCC usually presents as a red/ brown plaque or patch with a raised, thread-like edge, which is often best seen by stretching the skin; this helps to distinguish it from Bowen’s disease. Less commonly, a morphoeic, infiltrative BCC presents as an ill-defined, slowly enlarging, sclerotic yellow/grey plaque.

Management

Management involves early diagnosis and establish- ment of the correct treatment approach, taking into account patient and lesion factors (Box 28.16). Surgery is often the treatment of choice, although, increasingly, the place of non-surgical therapies is being recognised for low-risk BCC in patients in whom surgery is not appro- priate. For example, an early nodular BCC in a fit patient is best excised surgically, whereas large, multiple, super- ficial BCCs on the trunk of a frail elderly patient with comorbidities may be best treated by a non-surgical approach.

123
Q

What is squamous cell carcinoma?

A

Squamous cell carcinoma (SCC) is a malignancy that arises from epidermal keratinocytes and is the second most common skin cancer, occurring more frequently in elderly males and smokers.
Clinical features
SCC usually occurs on chronically sun-exposed sites, such as bald scalp, tops of ears, face and back of hands. The clinical presentation may be diverse, ranging from rapid development of a painful keratotic nodule in a pre-existing area of dysplasia (Fig. 28.10) to the de novo presentation of an erythematous, infiltrated, often-warty nodule or plaque that may ulcerate. The clinical appear- ance depends on histological grading; well-differentiated tumours more often present as defined keratotic nodules (see Fig. 28.10), whereas poorly differentiated tumours tend to be ill-defined and infiltrative, and may ulcerate. SCC has metastatic potential; some tumours, such as those on lip and ears and in immunosuppressed patients, behave more aggressively and are more likely to metas- tasise to draining lymph nodes.

Management
Early diagnosis is important and complete surgical exci- sion is the usual treatment of choice.

124
Q

What is actinic or solar keratoses?

A
Actinic keratoses (AK) are hyperkeratotic erythematous lesions arising on chronically sun-exposed sites. Histol- ogy shows dysplasia, although the diagnosis of typical AK is usually made on clinical grounds (Fig. 28.11). They are very common in fair-skinned people who have had significant sun exposure, are often multiple and increase with age. Prevalence is much higher in Aus- tralia than in the UK and some surveys have shown a prevalence of more than 50% in those over 40 years old. The rate of progression to SCC is less than 0.1% and spontaneous resolution is possible. However, SCC can also arise de novo and without progression from AK. Increase in size, ulceration, bleeding, pain or tenderness can be indicative of transformation into SCC.
					Management
A range of treatment options are available for AK (see Box 28.16). Emollients and photoprotection, including high-factor sunscreens, may suffice for mild disease. Single or low numbers of lesions of AK can be effec- tively treated with cryotherapy. Multiple lesions require field-directed therapy, such as 5-fluorouracil, imiqui- mod, diclofenac in hyaluronic acid, PDT or ingenol mebutate. Hyperkeratotic lesions may require curettage and cautery.
125
Q

What is Bowen’s disease?

A

Bowen’s disease (BD) usually presents as a slowly enlarging, erythematous, scaly plaque on the lower legs of fair-skinned elderly women but may occur at other sites (Fig. 28.12). It can be confused with eczema or pso- riasis, but is usually asymptomatic and does not respond to topical steroids. It may also be hard to distinguish from superficial BCC. Diagnostic biopsy shows intra- epidermal carcinoma but no invasion through the base- ment membrane. Transformation into SCC occurs in 3% or less.

126
Q

What is a keratoacanthoma?

A

Although benign, this squamous tumour is often diffi- cult to distinguish from SCC and is thus included in this section. It has a striking clinical presentation of rapid growth over weeks to months and subsequent spontane- ous resolution. It is thought to be associated with chronic sun exposure and most commonly occurs on the central face. The classical appearance is of an isolated dome- shaped nodule often of 5 cm or more in diameter, with a central keratin plug (Fig. 28.13). Clinically and histo- logically, the lesion often resembles SCC (see Fig. 28.10A); most are treated surgically, either by curettage and cautery or excision, to rule out SCC and to avoid the unsightly scar after spontaneous resolution.

127
Q

Describe the approach you would take to distinguish a mole from malignant melanoma.

A
A - Asymmetrical
B - Border
C - Colour
D - Diameter (larger than 6 mm)
E - Evolution
128
Q

What is diabetes mellitus?

A

Diabetes mellitus is a clinical syndrome that results from excessive levels of glucose in the blood (hyperglycaemia) caused by absolute or relative deficiency of insulin. Lack of insulin affects the metabolism of carbohydrate, protein and fat and can cause disturbance of water and electrolyte balance.
In control of blood glucose insulin has two important roles. Firstly it ensures the level of blood glucose never rises above a level that is healthy for the body. Secondly it enables cells to take up glucose from the blood.
The effects of diabetes are threatening to health in two broad ways, in acute diabetes an extreme lack of insulin causes high levels of glucose which results in dehydration and ketoacidotic coma. In chronic diabetes uncontrolled high levels of blood glucose have deleterious effects on various systems of the body particularly the eye, kidney and nervous system.

129
Q

What are the actions of insulin?

A

After a meal blood insulin levels increase, secreted from beta cells of the pancreas in response to rising blood glucose levels. Insulin lowers glucose by suppressing liver gluconeogenesis (synthesis of glucose), promoting glycogen synthesis, stimulating glucose uptake, particularly in skeletal muscle and fat, and promoting storage of muscle glycogen. Insulin stimulates synthesis of protein and fat (lipogenesis) and suppresses lipolysis (fat breakdown). Insulin controls the breakdown of protein to amino acids, oxidation of glucose to lactate and pyruvate, and formation of free fatty acids. In the absence of insulin there is gluconeogenesis from glycogen, glycerol, amino acids and lactate. (+stimulation by insulin –suppression by insulin)

130
Q

What is type 1 diabetes?

A

Type 1 diabetes is a T cell-mediated autoimmune disease resulting in destruction of the insulin secreting beta cells of the pancreas islets. It is also termed ‘insulin-dependent diabetes mellitus’ because of the patient’s absolute need for insulin replacement and used to be called ‘juvenile-onset diabetes’ as it primarily develops in children and young adults.
Genetic factors account for about one third of the susceptibility to type 1 diabetes with some overlap between genes associated with other autoimmune disease such as coeliac and thyroid disease.
Environmental factors have an important role in promoting clinical expression of the disease. One hypothesis is that reduced exposure to microorganisms in early childhood limits maturation of the immune system and increases susceptibility to autoimmune disease. Another hypothesis is a viral infection in the pancreas is a trigger by altering beta cell immunogenicity. Dietary factors may also be important.

131
Q

What are the sequences of metabolic events in insulin deficiency?

A

Insulin deficiency:
Increased glycogenolysis → Hyperglycaemia

Increased gluconeogenesis → Hyperglycaemia

Decreased uptake of blood glucose → Hyperglycaemia

Increased lipolysis → Increased Free Fatty Acids (FFA) and glycerol to liver → Ketogenesis → Metabolic acidosis

Hyperglycaemia:
Glycosuria → Osmotic diuresis → Dehydration → hyperosmolarity
Dehydration → Secondary hyperaldosteronism → K+ deficiency
Dehydration → Decreased renal function

132
Q

Explain why abdominal obesity and lack of physical exercise increase the incidence of type 2 diabetes.

A

Epidemiological studies show that type 2 diabetes is associated with overeating, especially when combined with obesity and underactivity. Middle-aged people with diabetes eat significantly more and are fatter and less active than their non-diabetic siblings. The risk of developing type 2 diabetes increases tenfold in people with a body mass index (BMI) of more than 30 kg/m2 (p. 115). However, although the majority of patients with type 2 diabetes are obese, only a minority of obese people develop diabetes, as the majority of obese patients are able to increase insulin secretion to compensate for the increased demand resulting from obesity and insulin resistance. Those who develop diabetes may have genet- ically impaired β-cell function, reduced β-cell mass, or a susceptibility of β cells to attack by toxic substances such as FFAs or inflammatory cytokines.

133
Q

Describe the roles of genetic and environmental factors in the development of type 2 diabetes.

A

Genetic factors are important in type 2 diabetes, as shown by marked differences in susceptibility in dif- ferent ethnic groups and by studies in monozygotic twins where concordance rates for type 2 diabetes approach 100%. However, many genes are involved and the chance of developing diabetes is also influenced very powerfully by environmental factors (Box 21.3). Genome-wide association studies have identified over 65 genes or gene regions that are associated with type 2 diabetes, each exerting a small effect. The largest effect is seen with variation in TCF7L2; the 10% of the population with two copies of the risk variant for this gene have a nearly twofold increase in risk of develop- ing type 2 diabetes. Most of the genes known to con- tribute to risk of type 2 diabetes are involved in β-cell function or in regulation of cell cycling and turnover, suggesting that altered regulation of β-cell mass is a key factor.

134
Q

What are the symptoms of hyperglycaemia?

A
  • Polyuria
  • Nocturia
  • Tiredness, fatigue, lethargy
  • Change in weight (usually weight loss) • Blurring of vision
  • Pruritus vulvae, balanitis (genital candidiasis) • Nausea
  • Headache
  • Hyperphagia; predilection for sweet foods
  • Mood change, irritability, difficulty in concentrating, apathy