paeds 2 ? Flashcards
triad of depression
Low mood
Anhedonia, a lack of pleasure in activities
Low energy
depression symptoms in youths
Low mood Anhedonia, a lack of pleasure in activities Low energy Anxiety and worry Clinginess Irritability Avoiding social situations (e.g. school) Hopelessness about the future Poor sleep, particularly early morning waking Poor appetite or over eating Poor concentration Physical symptoms such as abdominal pain
conservative management of depression
watchful waiting and advice about healthy habits, such as healthy diet, exercise and avoiding alcohol and cannabis.
moderate to severe depression treatment first line
Psychological therapy as the first line treatment with cognitive behavioural therapy, non-directive supportive therapy, interpersonal therapy and family therapy
first line antidepressant for depression in youths
Fluoxetine is the first line antidepressant in children, starting at 10mg and increasing to a maximum of 20mg
second line antidepressants for youth depression
Sertraline and citalopram
medical treatment timeline for depression
continue 6 months after remission is achieved
severity of anxiety can be assessed through
GAD-7 anxiety questionnaire, as well as co-morbidity and environmental triggers
mild anxiety treatment
watchful waiting and advice about self-help strategies (e.g. meditation), diet, exercise and avoiding alcohol, caffeine and drugs.
moderate to severe anxiety treatment
Counselling
Cognitive behavioural therapy
Medical management. Usually an SSRI such as sertraline is considered.
obsessions are
unwanted and uncontrolled thoughts and intrusive images
compulsions are
repetitive actions the person feels they must do, generating anxiety if they are not done.
features of autistic social interaction
Lack of eye contact Delay in smiling Avoids physical contact Unable to read non-verbal cues Difficulty establishing friendships Not displaying a desire to share attention
features of communication in autistics
Delay, absence or regression in language development
Lack of appropriate non-verbal communication such as smiling, eye contact, responding to others and sharing interest
Difficulty with imaginative or imitative behaviour
Repetitive use of words or phrases
behavioural features in autistic
Greater interest in objects, numbers or patterns than people
Stereotypical repetitive movements. There may be self-stimulating movements that are used to comfort themselves, such as hand-flapping or rocking.
Intensive and deep interests that are persistent and rigid
Repetitive behaviour and fixed routines
Anxiety and distress with experiences outside their normal routine
Extremely restricted food preferences
what key part of ADHD helps differentiate it from an enviromental problem?
consistent across all various settings
features of ADHD
Very short attention span
Quickly moving from one activity to another
Quickly losing interest in a task and not being able to persist with challenging tasks
Constantly moving or fidgeting
Impulsive behaviour
Disruptive or rule breaking
what is the type of medication used for treatment of ADHD
central nervous system stimulants.
examples of medication used in ADHD
Methylphenidate (“Ritalin“)
Dexamfetamine
Atomoxetine
pathology of anorexia
the person feel they are overweight despite evidence of normal or low body weight. It involves obsessively restricting calorie intake with the intention of losing weight.
features of anorexia nervosa
Excessive weight loss Amenorrhoea Lanugo hair is fine, soft hair across most of the body Hypokalaemia Hypotension Hypothermia Changes in mood, anxiety and depression Solitude
cardiac complications of anorexia include
arrhythmia, cardiac atrophy and sudden cardiac death.
the teenage girl with a normal body weight that presents with swelling to the face or under the jaw (salivary glands), calluses on the knuckles and alkalosis on a blood gas. The presenting complaint may be abdominal pain or reflux.. what is the underlying problem?
bulimia nervosa
features of bulimia nervosa?
alkalosis, due to vomiting hydrochloric acid from the stomach
Hypokalaemia
Erosion of teeth
Swollen salivary glands
Mouth ulcers
Gastro-oesophageal reflux and irritation
Calluses on the knuckles where they have been scraped across the teeth. This is called Russell’s sign.
binge eating disorder may involve
A planned binge involving “binge foods” Eating very quickly Unrelated to whether they are hungry or not Becoming uncomfortably full Eating in a “dazed state”
high risk for refeeding syndrome are those
if they have a BMI below 20 and have had little to eat for the past 5 days.
pathology behind refeeding syndrome
Metabolism in the cells and organs dramatically slows during prolonged periods of malnutrition. As the starved cells start to process glucose, protein and fats again they use up magnesium, potassium and phosphorus.
refeeding syndrome protocol
Slowly reintroducing food with restricted calories
Magnesium, potassium, phosphate and glucose monitoring along with other routine bloods
Fluid balance monitoring
ECG monitoring may be required in severe cases
Supplementation with electrolytes and vitamins, particularly B vitamins and thiamine
anxiety personality disorders
avoidant, dependent and obsessive.
Avoidant personality disorder features
severe anxiety about rejection or disapproval and avoidance of social situations or relationships.
Dependent personality disorder features
heavy reliance on others to make decisions and take responsibility for their lives, taking a very passive approach.
Obsessive compulsive personality disorder features
features unrealistic expectations of how things should be done by themselves and others, and catastrophising about what will happen if these expectations are not met.
Paranoid personality disorder features
features difficulty in trusting or revealing personal information to others.
Schizoid personality disorder features
features a lack of interest or desire to form relationships with others and feelings that this is of no benefit to them.
emotional impulsive personality disorder examples
borderline personality disorder, histrionic, narcissistic
Borderline personality disorder features
fluctuating strong emotions and difficulties with identity and maintaining healthy relationships.
Histrionic personality disorder features
features the need to be at the centre of attention and having to perform for others to maintain that attention.
Narcissistic personality disorder features
features feelings that they are special and need others to recognise this or else they get upset. They put themselves first.
examples of suspicious personality disorders
paranoid, schizoid and schizotypal.
key management of choice for a personality disorder
Cognitive behavioural therapy (CBT) and psychotherapy
Copropraxia refers too
involves making obscene gestures
Coprolalia refers too
involves saying obscene words
Echolalia refers too
involves repeating other people’s words
troublesome tics may be treated with
Habit reversal training
Exposure with response prevention
Medications may be tried in very severe cases, usually with antipsychotic medications
Fetal haemoglobin subunits are
two alpha and two gamma subunits.
adult haemoglobin subunits are
two alpha and two beta subunits.
foetal or adult haemoglobin has greater affinity?
foetal.
at birth the haemoglobin ratio is
At birth, around half the haemoglobin produced is HbF and half is HbA
what drug can be used to increase production of foetal haemoglobin in patients with sickle cell anaemia?
Hydroxycarbamide
foetal haemoglobin doesnt sickle because
is no beta subunit in the structure.
normal haemoglobin at birth?
150 – 235 grams/litre
normal haemoglobin at 2 months - 6 years
110 – 140 grams/litre
female haemoglobin 12-18
120 – 160 grams/litre
normal haemoglobin 12-18 male
130 -160 grams/litre
common cause on anaemia in infancy is
Physiologic anaemia of infancy
other causes of anaemia in infants is
Anaemia of prematurity
Blood loss
Haemolysis
Twin-twin transfusion
haemolytic causes of anaemia
Haemolytic disease of the newborn (ABO or rhesus incompatibility)
Hereditary spherocytosis
G6PD deficiency
normal dip in haemoglobin in infants occurs around
six to nine weeks
phsyiological anaemia of infancy is due to
High oxygen delivery to the tissues caused by the high haemoglobin levels at birth cause negative feedback. Production of erythropoietin by the kidneys is suppressed and subsequently there is reduced production of haemoglobin by the bone marrow.
common causes of Anaemia in older children is
Iron deficiency anaemia secondary to dietary insufficiency. This is the most common cause overall.
Blood loss, most frequently from menstruation in older girls
common cause of global chronic anaemia is
Worldwide, a common cause of blood loss causing chronic anaemia and iron deficiency is helminth infection, with roundworms, hookworms or whipworms.
causes of microcytic anaemia
T – Thalassaemia A – Anaemia of chronic disease I – Iron deficiency anaemia L – Lead poisoning S – Sideroblastic anaemia
causes of normocytic anaemia
A – Acute blood loss A – Anaemia of Chronic Disease A – Aplastic Anaemia H – Haemolytic Anaemia H – Hypothyroidism
causes of macrocytic megaloblastic anaemia
B12 deficiency
Folate deficiency
causes of normoblastic macrocytic anamia
Alcohol Reticulocytosis (usually from haemolytic anaemia or blood loss) Hypothyroidism Liver disease Drugs such as azathioprine
symptoms of anaemia
Tiredness Shortness of breath Headaches Dizziness Palpitations Worsening of other conditions
specific symptoms of iron deficiency anaemia
pica and hair loss
general signs of anaemia
Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate
specific signs of anaemia
koilonychia, angular chelitis, atrophic glossitis, brittle hair and nails, jaundice or bone deformities (thalassaemia)
initial investigations for anaemia
Full blood count for haemoglobin and MCV Blood film Reticulocyte count Ferritin (low iron deficiency) B12 and folate Bilirubin (raised in haemolysis) Direct Coombs test (autoimmune haemolytic anaemia) Haemoglobin electrophoresis (haemoglobinopathies)
iron is absorbed in the
duodenum and jejunum.
what form is iron absorbed in
ferrous (Fe2+) due to stomach acid.
ferric ions bind to what carrier?
transferrin
total iron binding capacity related to the amount of?
transferrin
transferring saturation =
Serum Iron / Total Iron Binding Capacity
extra ferritin may be released when there is
inflammation.
normal total iron binding capacity
54 – 75 μmol/L
what may give the impression of iron overload?
acute liver damage
what type of leukemia is most common?
Acute lymphoblastic leukaemia (ALL)
Acute lymphoblastic leukaemia commonly peaks at age
2-3
Acute myeloid leukaemia (AML) peaks age
under 2 years
what syndromes increases risk of leukaemia
Down’s syndrome
Kleinfelter syndrome
Noonan syndrome
Fanconi’s anaemia
presentation of leukaemia
Persistent fatigue Unexplained fever Failure to thrive Weight loss Night sweats Pallor (anaemia) Petechiae and abnormal bruising (thrombocytopenia) Unexplained bleeding (thrombocytopenia) Abdominal pain Generalised lymphadenopathy Unexplained or persistent bone or joint pain Hepatosplenomegaly
refer any child to haemotology for oncological assessmen if presenting with
unexplained petechiae or hepatomegaly
if leukaemia is suspected what test should be urgently performed?
FBc <48 hours
investigations for diagnosis of leukaemia should be
Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
Blood film, which can show blast cells
Bone marrow biopsy
Lymph node biopsy
staging investigations for leukaemia include
Chest xray
CT scan
Lumbar puncture
Genetic analysis and immunophenotyping of the abnormal cells
therapies for leukaemia are
chemotherapy.
Other therapies:
Radiotherapy
Bone marrow transplant
Surgery
key differential haematoligcal for non blanching rash
leukaemia or idiopathic thrombocytopenic purpura
ITP is an example of what type of hypersensitivity?
type II hypersensitivity reaction. It is caused by the production of antibodies that target and destroy platelets.
presentation of ITP is
Often there is a history of a recent viral illness. The onset of symptoms occurs over 24 – 48 hours:
Bleeding, for example from the gums, epistaxis or menorrhagia
Bruising
Petechial or purpuric rash, caused by bleeding under the skin
petechiae size
~1mm
purpura size
3-10mm
ecchymoses size
> 10mm
ix for ITP
urgent full blood count for the platelet count.
for severe bleeds with ITP treatment should be
may be required if the patient is actively bleeding or severe thrombocytopenia (platelets below 10):
Prednisolone
IV immunoglobulins
Blood transfusions if required
Platelet transfusions only work temporarily
sickle cell anaemia genetic transmission is via
autosomal recessive
what chromosome is effected with sickle cell anaemia
chromosome 11
complications of sickle cell anaemia
Anaemia Increased risk of infection Stroke Avascular necrosis in large joints such as the hip Pulmonary hypertension Painful and persistent penile erection (priapism) Chronic kidney disease Sickle cell crises Acute chest syndrome
general management of sickle cells anaemia?
Avoid dehydration and other triggers of crises
Ensure vaccines are up to date
Antibiotic prophylaxis to protect against infection, usually with penicillin V (phenoxymethypenicillin)
hydroxycarbamide
curative option for sickle cell anaemia?
bone marrow transplant
supportive management for a sickle cell crisis
Have a low threshold for admission to hospital
Treat any infection
Keep warm
Keep well hydrated (IV fluids may be required)
Simple analgesia such as paracetamol and ibuprofen
vaso-occlusive crisis may cause what in men?
priapism in men by trapping blood in the penis, causing a painful and persistent erection.
splenic sequestration crisis refers too
red blood cells blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen.
complication of splenic sequestration crisis is
circulatory collapse.
sickle cell aplastic crisis may be causes by
parvovirus B19
aplastic crisis refers too
temporary loss of the creation of new blood cells.
diagnosis of sickle cell acute chest syndrome requires.
Fever or respiratory symptoms, with:
New infiltrates seen on a chest xray
Tx for sickle cell acute chest syndrome is
Antibiotics or antivirals for infections
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Artificial ventilation with NIV or intubation may be required
both thalassaemia’s genetic inheritance are
autosomal recessive
signs and symptoms of thalassaemia
Microcytic anaemia (low mean corpuscular volume) Fatigue Pallor Jaundice Gallstones Splenomegaly Poor growth and development Pronounced forehead and malar eminences
diagnosis of thalassaemia is through
Full blood count shows a microcytic anaemia.
Haemoglobin electrophoresis is used to diagnose globin abnormalities.
DNA testing
risk of treatment with thalassaemia?
iron overload requiring iron chelation therapy
alpha thalassaemia is caused by defects on chromosome
16
beta Thalassaemia Minor means
they have microcytic anaemia with one normal beta and one abnormal beta gene
beta Thalassaemia Intermedia means
This can be either two defective genes or one defective gene and one deletion gene.
beta thalassaemia major means
homozygous for the deletion genes.
hereditary spherocytosis genetic transmission
autosomal dominant
presentation of hereditary spherocytosis
Jaundice
Anaemia
Gallstones
Splenomegaly
crises that may arise from hereditary spherocytosis
haemolytic, or aplastic
diagnosis of hereditary spherocytosis is through
family history and clinical features, along with spherocytes on the blood film. The mean corpuscular haemoglobin concentration (MCHC) is raised on a full blood count. Reticulocytes will be raised
management of hereditary spherocytosis is
Treatment is with folate supplementation and splenectomy. Removal of the gallbladder (cholecystectomy) may be required if gallstones are a problem. Transfusions may be required during acute crises.
a patient that becomes jaundice and anaemic after eating broad beans, developing an infection or being treated with antimalarial medications. The underlying diagnosis might be
G6PD deficiency
G6PD genetic transmission is
x-linked recessive
role of G6PD enzyme is
protect cells from damage by reactive oxygen species that may cause haemolysis during period of acute stress.
G6PD presentation
neonatal jaundice.
Other features of the condition are:
Anaemia
Intermittent jaundice, particularly in response to triggers
Gallstones
Splenomegaly
G6PD on blood film may show
Heinz bodies may be seen on a on blood film. Heinz bodies are blobs of denatured haemoglobin (“inclusions”) seen within the red blood cells.
diagnosis of G6PD may be through
enzyme assay
the skin sensitisation theory dictates allergy arises from
- exposure through breaks in the skin
2. lack of GI exposure to the allergen.
type 1 hypersensitivity involves
IgE antibodies to a specific allergen trigger mast cells and basophils to release histamines and other cytokines. This causes an immediate reaction.
type 1 hypersensitivity reaction involves
range from itching, facial swelling and urticaria to anaphylaxis.
type 2 hypersensitivity reaction pathology
IgG and IgM antibodies react to an allergen and activate the complement system, leading to direct damage to the local cells.
examples of type 2 hypersensitivity reactions are
haemolytic disease of the newborn and transfusion reactions.
type 3 hypersensitivity reaction involves
Immune complexes accumulate and cause damage to local tissues.
type 3 hypersensitivity reaction examples
systemic lupus erythematosus (SLE), rheumatoid arthritis and Henoch-Schönlein purpura (HSP)
type 4 hypersensitivity reaction pathology
Cell mediated hypersensitivity reactions caused by T lymphocytes. T-cells are inappropriately activated, causing inflammation and damage to local tissues.
examples of type 4 hypersensitivity reactions include
organ transplant rejection and contact dermatitis.
three main ways to test for an allergy are
Skin prick testing
RAST testing, which involves blood tests for total and specific immunoglobulin E (IgE)
Food challenge testing
RAST testing involves
measures the total and allergen specific IgE quantities in the patient’s blood sample
following exposure to an allergen treatment is
Antihistamines (e.g. cetirizine)
Steroids (e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone)
Intramuscular adrenalin in anaphylaxis
symptoms of anaphylaxis are
Urticaria
Itching
Angio-oedema, with swelling around lips and eyes
Abdominal pain
anaphylaxis can be confirmed by
measuring the serum mast cell tryptase within 6 hours of the event
why most children be observed post anaphylactic episode?
as biphasic reactions can occur, meaning they can have a second anaphylactic reaction after successful treatment of the first.
tryptase is released upon
cell degranulation
examples of non sedating antihistamines are
cetirizine, loratadine and fexofenadine
examples of sedating histamines are
chlorphenamine (Piriton) and promethazine
rapid reaction to cows milk indicates what ab mediated cows milk allergy
IgE mediated.
is cows milk intolerance an allergic process?
no
GI symptoms of cows milk allergy?
Bloating and wind
Abdominal pain
Diarrhoea
Vomiting
general allergic symptoms to cows milk protein
Urticarial rash (hives) Angio-oedema (facial swelling) Cough or wheeze Sneezing Watery eyes Eczema
management of cow’s milk allergy is with
Breast feeding mothers should avoid dairy products
Replace formula with special hydrolysed formulas designed for cow’s milk allergy. every 6 months tried on the milk ladder.
what are signs of recurrent infection that should prompt referral?
Chronic diarrhoea since infancy
Failure to thrive
Appearing unusually well with quite a severe infection, for example afebrile with a large pneumonia
Significantly more infections than expected, particularly bacterial lower respiratory tract infections
Unusual or persistent infections such as cytomegalovirus, candida and pneumocystis jiroveci
tests for recurrent infections should include
FCB, immunoglobulins, complement proteins, antibody responses, HIV, CXR, sweat test and CT (bronchiectasis)
SCID presentation is
Persistent severe diarrhoea
Failure to thrive
Opportunistic infections that are more frequent or severe than in healthy children, for example severe and later fatal chickenpox, Pneumocystis jiroveci pneumonia and cytomegalovirus
Unwell after live vaccinations such as the BCG, MMR and nasal flu vaccine
Omenn syndrom
more than 50% of SCID cases are due to
mutations in the common gamma chain on the X chromosome that codes for interleukin receptors on T and B cells
omen syndrome is the result of a mutation on
t is the result of a mutation in the recombination-activating gene (RAG 1 or RAG 2) that codes for important proteins in T and B cells.
omen syndrome genetic transmission is through
autosomal recessive
features of omen syndrome are
A red, scaly, dry rash (erythroderma) Hair loss (alopecia) Diarrhoea Failure to thrive Lymphadenopathy Hepatosplenomegaly
Tx of SCID involves
Ig therapy, sterile enviroment, avoiding live vaccines, and haematopoietic stem cell transplantation
what infections are particularly common with B cell and immunoglobulin disorders
LRTI
the most common immunoglobulin deficiency is
IgA
IgA protects
mucous membranes, such as saliva, respiratory tract secretions, GI tract secretions, tears and sweat.
Common Variable Immunodeficiency results in deficiencies in
IgG and IgA, with or without a deficiency in IgM.
DiGeorge Syndrome is also known as
22q11.2 deletion syndrome,
22q11.2 deletion syndrome leads to what embryological birth defect?
developmental defect in the third pharyngeal pouch and third branchial cleft.
with 22q11.2 deletion syndrome and the developmental defect in the third pharyngeal pouch and third branchial cleft what is the clinical relevance of this?
One of the consequences of this is incomplete development of the thymus gland. An underdeveloped thymus gland results in an inability to create functional T cells.
features of digeorge syndrome are
C – Congenital heart disease
A – Abnormal facies (characteristic facial appearance)
T – Thymus gland incompletely developed
C – Cleft palate
H – Hypoparathyroidism and resulting Hypocalcaemia
22nd chromosome affected
Purine Nucleoside Phosphorylase Deficiency genetic transmission
autosomal recessive
Purine Nucleoside Phosphorylase Deficiency pathology
NPase is an enzyme that helps breakdown purines. Without this enzyme, a metabolite called dGTP builds up. This metabolite is exclusively toxic to T cells
result of Purine Nucleoside Phosphorylase Deficiency is
Clinically, patients immunity to infection gradually gets worse. They become increasingly susceptible to infections, particularly viruses and live vaccines.
Wiskott-Aldrich Syndrome genetic transmission is
X-linked
Wiskott-Aldrich Syndrome results in
abnormal functioning T cells
Ataxic Telangiectasia genetic transmission
autosomal recessive
Ataxic Telangiectasia effects the gene coding for
ATM serine/threonine kinase protein - important for DNA coding
Ataxic Telangiectasia gene defect is on chromosome
11
Ataxic Telangiectasia features
Low numbers of T-cells and immunoglobulins, causing immunodeficiency and recurrent infections.
Ataxia: problems with coordination due to cerebellar impairment
Telangiectasia, particularly in the sclera and damaged areas of skin
Predisposition to cancers, particularly haematological cancers
Slow growth and delayed puberty
Accelerated ageing
Liver failure
complement proteins are important for what organisms
Haemophilus influenza B
Streptococcus pneumonia
Neisseria meningitidis
complement deficiency and SLE pathology
as an incomplete complement cascade leads to immune complexes building up and being deposited in tissues, leading to chronic inflammation.
what complement deficiency is the most common?
C2
bradykinin role in inflammatory response
promoting blood vessel dilatation and increased vascular permeability, leading to angioedema
C1 esterase role is to
inhibit bradykinin
absence of C1 esterase leads too
intermittent angioedema in response to minor triggers, such as viral infections or stress, or without any clear trigger at all.
test for hereditary angioedema (C1 esterase inhibitor deficiency) is to check
he levels of C4 (compliment 4). C4 levels will be low in the condition
mannose-binding lectin leads to inhibition of the
alternative pathway of the complement system.
examples of inactivated vaccines
Polio
Flu vaccine
Hepatitis A
Rabies
examples of subunit and conjugate vaccines
Pneumococcus Meningococcus Hepatitis B Pertussis (whooping cough) Haemophilus influenza type B Human papillomavirus (HPV) Shingles (herpes-zoster virus)
examples of live attenuated vaccines
Measles, mumps and rubella vaccine: contains all three weakened viruses
BCG: contains a weakened version of tuberculosis
Chickenpox: contains a weakened varicella-zoster virus
Nasal influenza vaccine (not the injection)
Rotavirus vaccine
8 weeks vaccine schedule
6 in 1 vaccin
meningococcal type B
Rotavirus (oral vaccine)
6 in 1 vaccine covers
6 in 1 vaccine (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B (Hib) and hepatitis B)
12 weeks vaccine schedule
6 in 1 vaccine (again)
Pneumococcal (13 different serotypes)
Rotavirus (again
16 weeks vaccine schedule
6 in 1 vaccine (again)
Meningococcal type B (again)
1 year vaccine schedule
2 in 1 (haemophilus influenza type B and meningococcal type C) Pneumococcal (again) MMR vaccine (measles, mumps and rubella) Meningococcal type B (again)
3 years vaccine schedule
4 in 1 (diphtheria, tetanus, pertussis and polio) MMR vaccine (again)
12-13 years vaccine schedule
Human papillomavirus (HPV) vaccine (2 doses given 6 to 24 months apart)
14 years vaccine schedule
3 in 1 (tetanus, diphtheria and polio)
Meningococcal groups A, C, W and Y
sepsis pathology leading from recognition to immune activation
by macrophages, lymphocytes and mast cells. These cells release vast amounts of cytokines, to alert the immune system to the invader. These cytokines activate other parts of the immune system. This immune activation leads to further release of chemicals such as nitrous oxide The immune response causes inflammation throughout the body.
examples of cytokines
such as interleukins and tumor necrosis factor
nitrous oxide causes
that causes vasodilation.
role of cytokines in sepsis
cause the endothelial lining of blood vessels to become more permeable. This causes fluid to leak out of the blood into the extracellular space, leading to oedema and a reduction in intravascular volume.
consequences of oedema in sepsis
The oedema around blood vessels creates a space between the blood and the tissues, reducing the amount of oxygen that reaches the tissues.
activation of coagulation system in sepsis pathophysiology
coagulation system leads to deposition of fibrin throughout the circulation, further compromising organ and tissue perfusion. It also leads to consumption of platelets and clotting factors, as they are being used up to form the blood clots.
the consumption of platelets and clotting factors in sepsis leads too and is overall called
his leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is called disseminated intravascular coagulopathy
the waste product of anaerobic respiration is
lactate
septic shock should be aggressively treated with
IV fluids
in ITU what drug is considered to aid in tissue perfusion during sepsis
inotropes (such as noradrenalin)
