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10- Swollen Leg > LOs > Flashcards

LOs Flashcards

1
Q

Describe the metabolic changes that occur in the rest-to-exercise transition (rest to light to moderate).

A

▪ ATP production increases immediately
▪ Increase in oxygen uptake rapidly
▪ Steady state is reached within one to four minutes
▪ During the transition there is an oxygen deficit (lag of oxygen uptake at the beginning of exercise)
▪ Oxygen deficit suggests that the anaerobic pathways contribute to the overall production of ATP early on in the process (ATP-PC system lasts around 1-5 seconds, Glycolysis)
▪ Once a steady state is reached -> body’s ATP requirement is met via aerobic metabolism.

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2
Q

Describe the changes in metabolism during recovery period following exercise

A

▪ Oxygen uptake remains elevated above rest
▪ There an oxygen debt (repayment for O2 deficit at onset of exercise
Excess post-exercise oxygen consumption (EPOC) - this is the period of breath fast and deep during exercise to return the oxygen levels to its pre-existing state

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3
Q

Describe the metabolic responses during short-term, high intensity exercise.

A

▪ 1-5 SECONDS = ATP produced via ATP-PC system
▪ >5 seconds = ATP production via glycolysis
▪ >45 seconds = ATP through ATP-PC, Glycolysis, and aerobic systems
▪ 60 seconds = 70/30 anaerobic/aerobic
▪ 2 minutes = 50/50

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4
Q

Describe the metabolic response to prolonged exercise lasting more than 10 minutes.

A

▪ ATP production primarily from aerobic metabolism

Steady oxygen state uptake can generally be maintained during submaximal exercise (below lactate threshold)

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5
Q

A) What is meant by VO2 max?

B) Name two physiological factors that may affect the VO2 max.

C) What ratio is used to estimate fuel utilization during exercise?

A

A) ▪ ‘Physiological ceiling’ or delivery of O2 to muscle
Affected by genetics and training

B) ▪ Maximum ability of cardiorespiratory system to deliver oxygen to the muscle
Ability of muscles to use oxygen and produce ATP aerobically

C) Respiratory Exchange Ratio (VCO2/VO2)
Ratio for fat = 0.7
Ratio for carbohydrates = 1.00

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6
Q

Name the fuel source that is used during low-intensity workouts (<30% VO2 max)

A

Fat (this is the primary source during long low intensity work outs)

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7
Q

Name the source that is used during high-intensity exercise (>70% VO2 max)

A

Carbohydrates are primary fuel source

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8
Q

Explain the ‘crossover’ concept.

A

Describes the shift from fat to CHO as exercise intensity increases
At around 30% VO2 max this shift occurs and carbohydrates become the main source of energy

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9
Q

Explain why there is a shift from fat to carbohydrates as exercise intensity increases.

A

Recruitment of fast muscle fibers

Increasing blood levels of epinephrine

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10
Q

Explain why low intensity workouts may not be the best for burning fat and losing weight although at such intensity fat is the primary source of energy.

A

Although high percentage of energy expenditure (-66%) derived from fat, the total energy expended is low
Higher intensities is low fat energy used but total enegy expended is higher

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11
Q

Describe the effect of exercise on resistance to infection (immune system.

A

Engaging in regular moderate (aerobic) exercise (40-60% VO2max - 20-40 minutes) = lower risk of URTI
Engaging in intense and/or long duration exercise (>90min) + people who do not exercise = higher risk

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12
Q

When could you advise a patient that they may continue to exercise if they are presenting to you with an infection?

A

If infection if above the neck (so symptoms like runny nose, nasal congestion, mild sore throat..)

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13
Q

List the mechanisms by which body heat is lost.

A

▪ Evaporation (heat from skin converts water to water vapor)
▪ Convection
▪ Conduction
Radiation

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14
Q

Describe the consequences of temperature above 45 degrees.

A

Destroy proteins and enzymes and leads to death

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15
Q

Describe the consequences of temperature under 34 degrees.

A

May cause slow metabolism d arrhythmias

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16
Q

Name the primary mechanism by which body heat is lost during exercise in a cool environment.

A

Evaporation

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17
Q

List Starling’s forces which govern the exchange of fluid between the capillary and the interstitial fluid.

A

▪ Hydrostatics pressure in the capillary (Pc)
▪ Hydrostatic pressure in the interstitium (Pi)
▪ Oncotic pressure in the capillary (pc)
▪ Oncotic pressure in the interstitium (pi)
(So Net Driving Pressure = [ (Pc - Pi) - (pc - pi) ])

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18
Q

List 4 causes of low albumin.

A

▪ Liver disease
▪ Nephrotic syndrome
▪ Malabsorption
▪ Protein losing enteropathy

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19
Q

At which end of the capillary bed is there net water movement into the interstitium

A

Arterial End due to higher capillary hydrostatic pressure than interstitial hydrostatic pressure.

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20
Q

Describe 4 pathological processes that can cause oedema.

A

▪ Reduction in plasma oncotic pressure (Cirrhosis (lower limb oedma + ascites), Nephrotic Syndrome (lower limb odema facial oedema) )
▪ Increase in capillary wall permeability infection/trauma - localised oedema)
▪ Increase in venous hydrostatic pressure (DVT (LOCALISED), Drugs (CCB), CHF (Reduction in CO -> Na and Water retention -> overloaded - Lower limb and raised JVP)
▪ Lymphatic blockage (Damage to lymphatics from radio therapy - localised)

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21
Q

List three symptoms you should ask about when screening for CHF in a patient with oedema.

A

▪ SOBOE
▪ Orthopnoea
▪ PND

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22
Q

List three symptoms you should ask about when screening liver disease.

A

▪ Malaise
▪ Anorexia
- Abdominal pain

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23
Q

List one feature of nephrotic syndrome that a patient may notice.

A

Frothy urine (due to hyperalbuminuria)

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24
Q

List drugs that can cause oedema.

A

▪ CCB
▪ NSAIDs
▪ Oestrogen (has effects similar to aldosterone leading to retention)
▪ Thiazolidinediones (glitazones) - these affect the Na-glucose transporter
▪ IV Fluids

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25
Q

List causes of pitting oedema.

A
  • Heart
  • Kidneys
  • Liver
  • Pregnancy (physiological usually)
  • Drugs

(Here there is oedema and fluid accumulation in the interstitial space however the lymph drainage system is functioning properly)

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26
Q

List causes of non-pitting oedema

A
  • Lymphoedema (tumour, infection, or congenital - here the lymph nodes are not functioning or not properly)
  • Myxedema - in condition like hypothyroidism, this occurs in legs, ankles but also eyelids and tongue on some occasions
  • Lipedema - fat cells grow and fill up with fluid, this is a painful case of oedema
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27
Q

Describe the investigations of Oedema.

A

▪ Urine dip - protein and blood check –> nephrotic syndrome?
▪ Bloods - FBC, U+E/eGFR, Liver function test (albumin), d-drimer (suspected clot)
▪ ECG - features of heat failure
▪ Imaging - CXR (EFFUSION), Liver USS, Duplex USS
▪ Echocardiogram

28
Q

A) Define the term nephrotic syndrome.

B) Describe the nephrotic range proteinuria as it is demonstrated on dipstick, ACR, PCR.

A

A)
▪ Oedema
▪ Proteinuria >3.5g/24h
▪ Hypoalbuminaemia

B)
▪ Dipstick = ++++
▪ ACR = >300
▪ PCR = >350

NOTE: Nephrotic syndrome is always due to glomerular disease. What differentiates it from tubular diseasei is that degree of proteinuria. (much higher in nephrotic/glomerular disease)

29
Q

List 3 Primary kidney diseases which cause Nephrotic syndrome.

A

▪ Minimal change disease
▪ Focal Segmental Glomerulosclerosis
▪ Membranous glomerular nephritis

30
Q

List two systemic diseases which could cause nephrotic syndrome.

A

▪ Diabetes

▪ Amyloid

31
Q

Name the three complications of nephrotic syndrome.

A

▪ Hypercholesterolaemia
▪ Hypercoagulability
▪ Infection

32
Q

Nephrotic syndrome treatmen?

A

1- Underlying cause (HF, if it is caused by minimal change mainlyin children use prednisolon, and can use ACE-I which has an anti-proteinuric)
2- Treat oedema
- if the cause if hypertension use this first, using furosemide)
3- Prevent coagulation issues

33
Q

List DD of SOB with minutes onset time.

A 
▪ PE
	▪ Pneumothorax
	▪ Acute LVF (due to infection, allergy, PE, Arrhythmias, MI)
	▪ Acute asthma
	▪ Inhaled foreign body
34
Q

List DD of SOB with hours to days.

A

▪ Pneumonia
▪ Asthma
▪ Exacerbation of COPD

35
Q

List DD of SOB weeks to months onset.

A

▪ Anaemia
▪ Pleural effusion (CHF, Cirrhosis, chronic infection)
▪ Respiratory neuromuscular disorder

36
Q

List DD of SOB with months to years onset.

A

▪ COPD
▪ Pulmonary fibrosis
○ There are many types, usually idiopathic, it is disease of interstitial space, usually fibrosis and inflammation (so can release blood)
○ Sx: SOB, dry cough, clubbing, tiredness, gradual unintentional weight loss
▪ Pulmonary TB (Bacterial infection, can be else where in the body but when it is in the lungs it is called pulmonary TB, spread through droplets, productive cough that may be bloody)

37
Q

What is the differential diagnosis for haemoptysis.

A

a. PE
b. Lung carcinoma
c. Pneumonia
d. TB
e. Vasculitis
f. Foreign body
g. Medications - anticoagulants

** ANY ONE 40 OR OVER WITH UNEXPLAINED HAEMPTYSIS SHOULD BE REFERRED FOR AN X-RAY WITHIN 2 WEEKS

38
Q

Hoarseness of voice DDx.

A 
▪ Infectious
		○ Laryngitis
	▪ Malignant
		○ Laryngeal carcinoma
		○ Lung Carcinoma (SOB, Hoarseness of voice, cough, tiredness, clubbing, weight loss)
	▪ Benign
		○ Vocal cord nodules
	▪ Neurological
		○ Stroke
		○ Motor neuron disease
	▪ Other
		○ Functional dysphonia

***Anyone aged 45 and over with hoarseness of voice should be referred

39
Q

DDx for stridor.

A 
DDx:
	▪ Extra thoracic
		○ Goiter 
		○ Lymphadenopathy
		○ Mediastinal tumors
	▪ Intra thoracic
		○ Narrowing of the airway (epiglottitis, anaphylaxis, retropharyngeal abscess) 
		○ Laryngospasm
		○ Foreign body inhalation
	▪ Trauma
40
Q

Describe the cycle of the lymph.

A

▪ Due to differences in pressures between arterial end and venous end, fluid leaves the arteries (20L)
▪ 17L reabsorbed by venous
▪ 3L absorbed by lymph vessels (thin-walled endothelial tubes)
▪ Lymph fluid is also made of other debris from dead cells and antigen-presenting cells
▪ Reaches the lymph nodes which act as filters (here the antigen-presenting cell present the antigen to the lymphocytes)
▪ After reaching the filter the lymph goes back into the venous side of the circulation

41
Q

Explain what is meant by sentinel lymph node sampling/biopsy

A

▪ If you can identify the first node involved in the drainage of a tumour, and sample it, If that’s not involved then there wont be spread of tumour into other lymph nodes.
▪ You can inject some fluorescent signal or radioactive substance into tumour, then that will be carried into the lymph node, the first node to receive that is called the sentinel node.

42
Q

Where does the right side of the head, neck and the right limb lymph vessels drain into?

A

▪ Right Lymphatic Duct

43
Q

A patient presents to their GP with swollen nodes in his arm and fever that have developed over the last 24 hours. He states that the only other symptoms he has is some pain in his left arm where a splinter had went in.

A) What sign would you expect to see up the patient's arm?

B) State a potential diagnosis.
A

A) What sign would you expect to see up the patient’s arm?
Red streak

B) State a potential diagnosis.
Lymphangitis
44
Q

List three pathogens that may cause systemic infections that lead to lymphadenopathy.

A

EBV (Risk factor in Hodgkin’s Lymphoma)
CMV
HIV or toxoplasma

45
Q

A mother presents to their GP worried that her 3 year old son has had swollen nodes in his neck for the last week with a rash over the flexor regions in his arms and legs that he keep itching. You examine the lesions and notice dry patches with erythematous background, and some crusting. What is the likely cause of the lymphadenopathy?

A

nflammatory lymphadenopathy due to undiagnosed eczema (due to pathogens and foreign bodies entering the boy through the broken skin)

46
Q

Name potential autoimmune causes of lymphadenopathy.

A

▪ Rheumatoid Arthritis

▪ SLE (Lupus)

47
Q

Name the disease: causes inflammatory lymphadenopathy, and cough/breathlessness which is due to granulomas (lesions) form mainly in the skin, lungs, and lymph nodes.

A

▪ Sarcoidosis

48
Q

Name a rare lymphoproliferative disorder that causes lymphadenopathy.

A

Castleman’s disease (Human Herpes Virus-8 (HHV8) associated) - abnormal growth of cells that is not cancerous in the lymph nodes.

49
Q

Describe the features of Primary Lymphoproliferative Disease. (Malignant Lymphoma).

A

▪ Rubbery, mobile, non-tender nodes - local/systemic
▪ May present with B symptoms:
• fever to 38C
• Drenching sweats (This is due to fluctuations in temperature)
• weight loss >10% in <6 months
▪ FBC - may have Chronic Lymphocytic Leukemia
▪ Lactate Dehydrogenase - non specific marker of cell turnover which can increase due to various reason including exercise and other cancers
▪ FNA usually insufficient and need more like an exicison or core biospy

50
Q

Describe the investigations that maybe used for lymphoma staging.

A 
▪ Physical Examination
▪ Chest X-Ray
▪ CT
▪ MRI  if bone or CNS concerns
▪ PET-CT : Glucose is labelled with a Radioactive substance, active disease takes up the glucose. So someone may have stage two Hodgkin's based on CT, but you see that there is some activity in neck, chest and abdomen, so they may then be upstaged - PET is like a functional CT
51
Q

What are the two functional anatomical areas of the spleen?

A

▪ Red Pulp - sinuses lined by macrophages which receives red cells
▪ White pulp - similar to lymph node - receives plasma and white cells

52
Q

Describe the Spleen’s Functions.

A

▪ Red cell phagocytosis - for example, old, damaged, antibody coated red blood cells
▪ Site of hemopoiesis in foetus but this changes to the marrow as the child gets older - used if additional space is needed
▪ Acts as a lymphoid organ (so just like a big lymph node!!)Blood pooling - platelets>red blood cells

53
Q

Splenomegaly causes are usually related to the function, but may also be related to the anatomy around the spleen. List 3 functions of the spleen with an example of their related disorder.

A

▪ Function as a lymphoid organ
• Things that cause lymphadenopathy can also cause splenomegaly here
• Additionally - Malaria (fever, vomiting, headache, jaundice) and other tropical causes
• Felty’s Syndrome - this describes splenomegaly with e.g. lupus or rheumatoid arthritis

▪ Function as a reticuloendothelial organ
• Site of red cell destruction so, any cause of haemolysis
• Storage disorders such as Gaucher Disease - genetic disorder where a subtype of glycolipids accumulate in cells and organs such as the marrow and spleen
• Amyloid

▪ Function as a hemopoietic site
• 20% newborns have palpable spleen before medulla of bone takes over
• Chornic myeloid leukaemia
• Myeloproliferative disorders eg primary polycythaemia, myelofibrosis
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54
Q

Provide an example of a cause of splenomegaly that relates to its anatomy.

A

▪ Cirrhosis (hepatic)
▪ Portal vein thrombosis (Pre-hepatic)
▪ Severe right heart failure (pre-hepatic)

55
Q

How do you investigate splenomegaly?

A
  • History
  • Exam
  • Simple bloods
  • Imaging
  • Bone Marrow
  • Splenic Biopsy
56
Q

List the classifications of PE.

A

▪ Massive - shock or hypotension
▪ Submassive - pulmonary trunk or main PA but not shocked
▪ Small - lobar or segmental

57
Q

When do you suspect a patient has PE.

A 
▪ Clinical symptoms:
		○ Dyspnoea
		○ Pleuritic chest pain 
		○ Cough 
		○ Fever
		○ Haemoptysis 
		○ (SIGNS: Tachycardia, tachypnoea, hypoxia etc…)
58
Q

You suspect a patient has a PE, describe the rest of the diagnostic process.

A

▪ Assess the likelihood of a PE through using different criteria (Wells Score, Revised Geneva Score, and Pulmonary Embolism Rule Criteria)

1- Well Score equal or less than 4 - if no you carry out a CTPA! to confirm or exclude a PE
2- PERC = 0 ? if yes PE excluded, if no…
3- D-Dimer - is it <500? PE excluded. If no then you do a CTPA

59
Q

When do you request a D-Dimer?

A

When the assessed risk of a PE is low

60
Q

What is a D-Dimer?

A

Fibrin degradation product

Represents a hypercoagulable state

61
Q

What is the upper limit of D-Dimer? And what happens to this value as a person gets older?

A

500mcg/L

Rises with age (need to keep this in mind)

62
Q

Describe one weakness of using the D-Dimer test as a diagnostic tool for PE.

A

Low specificity for VTE or any other disease -> high false positives -> unnecessary testing using radiation (CTPA)

63
Q

Describe the ECG pattern of a patient presenting with a PE.

A

RV strain pattern (T wave inversion in V1-V4 + T wave inversion in III and aVF - T wave inverios in ACS is also found but only in V1-V4)
Note: this pattern can be caused by other conditions such as chronic respiratory disease including COPD, interstitial Lung disease and OSA.
TAKE HOME POINT: PATIENTS WITH ACUTE SHORTNESS OF BREATH, NO PREVIOUS CARDIORESPIRATORY DISEASE, HYPOXAEMIA, NORMAL CXR AND RV STRAIN PATTERN ON THEIR ECG SHOULD BE TREATED AS PE UNTIL PROVEN OTHERWISE!

64
Q

Describe other potential ECG findings of a patient with PE aside from RV Strain pattern.

A

Sinus tachycardia (>100)
RBBB (Right bundle branch block) - QRS duration >120ms
Right axis deviation (Dominant S wave lead I with dominant R wave lead II and III)
Atrial tachyarrhythmias

65
Q

Describe the thrombolysis of a massive PE (saddle PE).

A

Systemic thrombolysis therapy (recommended for massive PE with sustain hypotension (<90mmhg)) for at least 15 minutes
Alteplase (tPA) 100mg IV over two hours
Stop anticoagulant during Alteplase infusion
Check APTT when infusion is complete
Restart unfractioned heparin when APTT <2x ULN
High risk of bleeding

66
Q

List a differential diagnosis of pleuritic pain (localised, sharp/stabbing chest pain that is exacerbated by inspiration).

A

PE
Pneumonia (cough, purulent sputum, fever, dyspnoea, pain, confusion in elderly
Pneumothorax (sudden pain, dyspnoea, hyperexpanded + hyperresonance on percussion on the side of the pneumothorax + diminished breath sounds compared to healthy side)
Pericarditis
Costochondritis (inflammation of the cartilage in the rib cage)
Intercostal myalgia (intercostal muscle pain)

10- Swollen Leg (1 decks)

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