Miscellaneous Flashcards
(185 cards)
What is a granuloma?
A collection of macrophages (as few as 4).
They often fuse and form Giant Cells
What is a non-caseating granuloma?
A non necrotising granuloma
What causes hereditary and acquired angioedema?
Caused by a deficiency or dysfunction of the C1 inhibitor.
This results in increased levels of bradykinin because C1 inhibits activated kallikren (required for the generation of bradykinin) in the kinin system pathway.
C1 inhibitor is a protein that regulates the classical complement pathway.
Explain about Hereditary Angioedema
Autosomal Dominant
2 types:
1= 80% inadequate C1-inhibitor production
2= production of dysfunctional C1-inhibitor
C1 inhibitor functional tests are abnormal in both, in type 2 C1 inhibitor levels are normal.
Kinins generated secondary to complement activation play a role in vascular leakage contributing to angio-odema.
usually presents during childhood or adolescence.
Explain about Acquired Angioedema
C1-inhibitor may be excessively consumed by : clonal B lymphocyte proliferation ( B-cell lymphoma) or massive immune complex type disease.
May also be caused by autoantibodies that block or interfere with otherwise normal C1-inhibitor function.
Distinguished from HAE by late adult onset, non-familial and with reduced levels of C1q
What are the triggers for Hereditary and Acquired Angioedema?
Injury/infection surgery/dental treatment stress pregnancy certain medications like the contraceptive pill
What are the symptoms for Hereditary and Acquired Angioedema?
Non-pruitic, recurrent, angio-oedematous swellings.
Common sites being- lips, tongue.eyelids,larynx and GI tract
Manifestations that suggest intestinal obstruction include N&V and colicky discomfort/
Bronchospasms don’t occur but laryngeal oedema may be present causing stridor.
What is the aetiology of Idiopathic Intracranial Hypertension?
Unknown
Highly associated with females and obesity (esp recent weight gain)
What is the pathophysiology of Idiopathic Intracranial Hypertension?
CSF absorption occurs both via the arachnoid granulations and along nerve root sheaths, especially along the olfactory nerve (cribform plate)
Thought that there is an increase in resistance to CSF outflow along one or both pathways.
What is the characteristic of Idiopathic Intracranial Hypertension?
Raised Intracranial Pressure in an alert, orientated patient without localising neurological findings or an obvious cause
What are the clinical features of Idiopathic Intracranial Hypertension?
Headache= severe, pulsatile, daily and may awaken pt.
Nausea Common
Neck and Shoulder Pain
Transient Visula Obscurations= episodes of transient grey/brown outs that last <30secs. they can be mono or bi-ocular. Thought to be transient ischaemia of the optic nerve.
Pulse-synchronous Tinnitus= 60% patients. Specific. Sound is often unilateral- jugular pressure ipsilateral to the sound abolishes it.
How do you manage Idiopathic Intracranial Hypertension?
1) Elimination of causal factors = weightloss
2) Acetazolamide (except 1st trimester of pregnancy)
+ Persistant headache= naproxene or amitriptyline or CSF shunting
+ Progressive visual loss= optic nerve sheath fenestration or CSF shunting
What is Cushing’s Reflex?
Bradycardia, Systolic Hypertension and Cheyne-Stoke respiration (irregular)
How does Cushing’s reflex occur?
In response to raised intracranial pressure
Causes+ primary/met tumour, head injury, haemorrhage, infection, hydrocephalus,cerebral oedema, status epilepticus.
Can also get if LP performed when there is a raised intracranial pressure ( except in IIH)
can also result from a low cerebral perfusion pressure (<15mmHg)
Mechanism of action of Cushing’s reflex?
1) ICP>MAB therefore get cerebral arteriole compression=cerebral ischaemia. In response to ischaemia you get sympathetic stimulation of arteries= constrict. This increases total resistance and increases MAB to try and restore bloodflow to the brain. Increase HR and CO
TACHYCARDIA AND HYPERTENSION
2) Baroreceptors in aortic arch detect raised BP and trigger parasympathetic response via vagus nerve (ICP may also distort vagus nerve and directly stimulate this pathway).
This induces BRADYCARDIA
3) Raised ICP causes increased pressure on the brain stem. Changes homeostasis and causes irregular breathing patterns.
What is a hernia?
The protrusion of a viscus into an abnormal space
What is a direct inguinal hernia?
Caused by a weakness in posterior wall of the inguinal canal.
Abdo contents forced through defect and into the canal
Hernia emerges medial to the deep ring canal (mid-point between ASIS and PT)
What is an indirect hernia?
Does not pierce posterior wall of the canal. The contents pass through the deep ring and exit via the superficial ring.
If you reduce the hernia and then press on the deep ring and get the patient to cough the hernia doesn’t re-emerge.
What is a femoral hernia?
The abdominal contents pass inferior to the inguinal canal and emerge in the femoral canal ( within the femoral sheath, medial to the artery and vein)
Space is tight and it is bordered medially by the edge of the lacunar ligament.
Increased risk of obstruction and strangulation.
How to you calculate maintenance fluid for children?
1st 10kg = 4ml/kg/hr or 100ml/kg
2nd 10kg = 2ml/kg/hr or 50ml/kg
all other kg= 1ml/kg/hr or 25ml/kg
+ ongoing losses
measured and replaced 4hrly
What is normal urine output for a child?
1ml/kg/hr
what is normal urine output for an adult?
0.5ml/kg/hr
What is an ALTE?
Apparent Life Threatening Event.
Apnoea that lasts over 30 seconds
What are the causes of Apnoea?
1/3 unknown
1/3 GORD
1/3 Other= RSV (prem), seizure, sepsis, pertusiis, sub-dural ( shaken baby)
Normal stop after 6 months. If they haven’t consider epilepsy or NAI