Transcript All of medicine in 12 hours…

The rest of medicine in six
hours
Dr. Alan McLeod (F2)
The Plan
Day One
Day Two
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A systematic approach
Chest Pain
Palpitations
Acute sob
Chronic sob
Haemoptysis
Painful Limb
TATT
Swallowing
Change in bowel habits
Hepatomegaly
Abdo pain
Pregnancy
Congenital abnormality
Head Injury
Emergency Management
Maximising your marks
I GET VINO…
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G
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T
V
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N
O
Infectious / inflammatory
Genetic / Idiopathic
Endocrine
Trauma
Vascular
Iatrogenic / ingested
Neoplastic
Organs / Other
2 Minutes
10 Reasons to be Tired All The
Time
TATT? Wine? For Me? Why
Not?
I
G
E
T
V
I
N
O
Infectious / inflammatory Multiple sclerosis, TB
Genetic / ideopathic
Endocrine
Diabetes, Hypothyroid
Trauma
Vascular
Anaemia
Iatrogenic / ingested
Neoplastic
Lymphoma, leucaemia
Organs / other
Depression, obesity, lifestyle
Anaemia
Erythrocytes
• Deformable
biconcave discs
Each carries
• 250 MILLION Hb
mols
• 1 billion O2 molecules
Anaemia – two classifications
Three basic causes
Three basic cell sizes
• Blood loss
• Reduced erythrocyte
production
• Increased erythrocyte
destruction
• Microcytic
• Normocytic
• Macrocytic
microcytic anaemia
normocytic anaemia
macrocytic anaemia
MCV < 76 femtolitres
MCV = 76-95 fL
MCV > 96 femtolitres
iron deficiency
anaemia of chronic
With megaloblastic
anaemia –commonest disease – commonest haemopoiesis on bone
marrow examination
lead poisoning
Acute haemorrhage
B12 deficiency
Sideroblastic anaemia Haemolytic anaemia
Folate deficiency
Thalassaemia
Bone marrow failure
(aplastic anaemia)
Anaemia of chronic
With normoblastic
disease
Mixed iron and folate
BM
Pyridoxine-responsive Pregnancy
anaemia
chronic renal failure
riboflavin deficiency
Alcohol
Liver cirrhosis
Hypothyroidism /
myxoedema
Protein Basics
Protein Basics
Protein Basics
Primary Structure
• Amino acid sequence
Secondary Structure
• Folded primary
structure
– Alpha helix
– Beta pleated sheet
Tertiary Structure
• Complex of
secondary structures
Quaternary structure
• Associated tertiary
structures
– e.g. Haemoglobin
Tissues
Fractual Concentration
1.0
Lungs
Myoglobin
Haemoglobin
0
pO2 (torr)
100
Bohr effect and 2,3-BPG
100%
[oxyhaemoglobin]
Right Shift
Easier to release O2
pH (e.g. lactic acid)
pCO2 (e.g. COPD)
temp (e.g. exercise)
2,3-BPG (e.g. altitude
training)
0
Left Shift
Reverse of these
pO2
10kPa
Bohr effect: CO2 pH
Haemoglobin is Allosteric
2,3-BPG
T-Form
• Bloomin’ – 2,3-BPG
can bind
• Tired – has no O2
R-Form
• Has enough O2 to
Run
Thallasaemia
• One gene encodes
the alpha globin
• Two genes encode
the beta globin
• Beta thallasaemia
minor = one gene
faulty
• Beta thallasaemia
major = both genes
faulty
Comparison of Inheritance
Modes
Autosomal
Dominant
Autosomal
Recessive
X-linked
Dominant
X-linked
Recessive
M=F
M >> F (almost
exclusively M)
2F : 1M
M >> F (almost
exclusively M)
Transmitted by
both sexes
Trans by carrier
females
Transmitted by
both sexes
Trans by carrier
females
MM
transmission
occurs
NO M M
transmission
NO M M
transmission
NO M M
transmission
Successive
generation
affected
Phenotype may
skip generations
Successive
generation
affected
All daughters of
affected M are
carriers
Iron Uptake & Storage
Iron is a vital element for
life
• Humans have no active
way of excreting iron
• 1-3 g stored
• 80% in haemoglobin
• 1 g lost / day from skin /
mucosal shedding
• 1 g lost / day extra in
menstruation
Absorbed
• Duodenum + upper
jejunum
• Exact mech unknown
• About 10% of intake
• Lead toxicity reduces
• Vit C increases
Important Molecules
• Transferrin
• Ferritin
•
•
•
•
•
•
•
•
Small
Extracellular
Transporter
Holds 1 or 2 iron
Large
Intracellular
Storage molecule
Up to 45,000 iron
CKD and EPO
Erythropoietin
• Glycoprotein
• 10% from liver
• 90% from kidneys
• Acts at bone marrow
• Renal cortex
• Peritubular capillary
endothelium
• Chronic Kidney
Disease
– Responds to low O2
– Promotes erythrocyte
production
– Promotes
haemoglobin synthesis
– Erythropoietin 
– Vitamin D 
– Renin 
B12 and Folate
Involved in
• RBC production
– Reduced RBC
numbers
– Increased size
– Reduceed O2 carrying
• DNA Sythesis
• Tissue regeneration
Pernicious Anaemia
• B12 deficiency
• B12 absorbed via
intrinsic factor
• IF produced by
Parietal cells in
stomach
B12 from food
R
R: Non-specific B12
binding protein
IF: Intrinsic factor
TC: Transcobalamin
R.B12
R
IF
Brush border
Parietal cells
Terminal
Ileum
TC
TC.B12
TC
B12
TC.B12
IF
IF.B12
Blood
Tissue
Cell
Diabetes
• Pancreatic Islets
• 60% beta cells
– Secrete insulin
• 25% alpha cells
– Secrete glucagon
• Reciprocal action of
hormones
– Not usually present
together
• Secretions enter
pancreatic vein into
portal system
Diabetes
Type 1
• Childhood
• Failure insulin prod.
• Insulin dependent
Type 2
• Traditionally older
• Insulin resistance
• Lifestyle/drugs/insulin
Insulin
Peptide hormone
• Alpha chain
– Species specific
• Beta chain
– Biologic activity
• C-peptoid joins chains
Packaging and Release
Insulin production
• Increased by glucose
– Transcription
– Translation
• Pre-proinsulin
– Signal peptide cleaved
• Packaged in Golgi into
secretory granules
– Insulin
– C-peptide
• Insulin forms hexamers
• Proinsulin
– Disulphide links
– Excision of C-peptide
• Insulin
• Secreted via exocytosis
Describe the modifications
that transform proinsulin into
insulin
Insulin
‘C’ Peptide
‘B’ Chain
‘A’ Chain
S
S
S
S
S
S
Insulin
‘C’ Peptide
‘B’ Chain
‘A’ Chain
S
S
S
S
S
S
Insulin
‘B’ Chain
‘A’ Chain
S
S
S
S
S
S
Release of Insulin
• GLUT-2 admits glucose
– Keeps intracellular conc
same as interstitial fluid
•
•
•
•
•
ATP prod stimulated
ATP:ADP ratio changes
ATP binds to K+ channel
Channel closes
Cell depolarisation
• Depolarisation
– Opening of voltage
gated Ca++ channels
– Increased [Ca++]
• Exocytosis
– Release of insulin
Insulin Stimulated Glucose Uptake
A
B
Glucose Transporters
GLUT 1
GLUT 3
GLUT 4
Not insulin
dependent
Not insulin
dependent
Insulin Dependent
Low Affinity
High Affinity
Low Affinity
Basal glucose
uptake for
respiration
Energy supply to
brain
Insulin related
glucose storage
Foetal Tissues
Adult RBCs
Low levels all
tissues
Neurons
Skeletal muscle
Cardiac Muscle
Adipose Tissue
Functions of Insulin
Anabolic
• Promotes glucose
uptake
• Promotes use of
glucose as a fuel
•
•
•
•
•
• Promotes K+ uptake
• Decreased proteolysis
• Decreased lipolysis
• Decr. gluconeogenesis
– Used to treat
hyperkalaemia
Protein synthesis
Blood proteins
Muscle tissue
TAG synthesis
Glycogen synthesis
Sulphonylureas
Insulin
Vesicle
Beta
Cell
K+
SUR1
K+
SUR1
Insulin Vesicle
Sulphonylurea Molecules
K+
SUR1
K+
SUR1
Insulin Vesicle
Sulphonylurea Molecules
Rising K+
SUR1
SUR1
Insulin Vesicle
Sulphonylurea Molecules
Ca++
Ca++
Ca++
Ca++
Ca++
Ca++
Depolarisation
Ca++
Ca++
SUR1
Ca++
SUR1
Ca++
Ca++
Insulin Vesicle
Sulphonylurea Molecules
Ca++
Ca++
Ca++
Insulin
Ca++
Ca++
SUR1
Ca++
Ca++
Ca++
SUR1
Ca++
Ca++
Other Drugs
Metformin
• Unknown mechanism
•  Gluconeogenesis
•  Insulin sensitivity
• No weight gain
• Epigastric discomfort
• Diarrhoea
• Anorexia
Glitazones
• Alpha ketoglutarase
inhibitor
•  carbohydrate
breakdown in gut
• Abdominal discomfort
• Diarrhoea
• Flatulence
2 Minutes
10 Causes of Abdo Pain
Phases of swallowing
Oral
Pharyngeal
Oesophageal
Bolus molding
Glottis closes
Larynx elevates
Food is deposited
into the
oesophagus
Peristaltic wave
takes bolus
downwards
Glottis opens
The nerves involved in swallowing are:
• CN IX: Glossopharyngeal
• CNX: Vagus
• CNXII: Hypoglossal
Dysphagia: difficulty in swallowing
By location
• Inside lumen
– Foreign body
– Tumour
• Within wall:
– Stricture
– Achalasia
• Outside oesophagus
– Lymphoma
– Lung cancer
By Mechanism
• Motor causes:
– Achalasia
• Mechanical causes:
– Tumour
– Stricture
– Foreign body
• Neurological:
– Bulbar palsy
– Myasthenia gravis
Achalasia
• Damage to myenteric
plexus
• Loss of peristalsis
• Inability of lower
oesophageal
sphincter to relax
• Barium swallow
• Balloon dilatation
Myasthenia Gravis
• Acquired autoimmune
– Thymic hyperplasia
75%
– Thymoma 15%
• Non-thymoma
– Two peaks
– 10-30 yrs F>M
– 60-70 yrs M>F
• Thymoma
– 40-50 yrs
Features
• Muscle weakness and
fatigueability, esp:
–
–
–
–
Periocular
Facial
Bulbar
Girdle
Normal Signal
Myasthenia Gravis
Cholinergic
Neurone
Cholinergic
Neurone
Normal Response
Acetylcholine
ACh receptor
Response Blocked
Anti AChR
Defecation
• Mass movement into
rectum
• If critical mass of stool in
rectum  distension of
rectal walls:
• Defecation sensation
• Defecation reflex
• Contraction rectum
• Relaxation int sphincter
• Contr. Ext sphincter
If convenient
• Increased pressure in
rectum  relaxation of
ext sphincter + expulsion
of faeces.
If not convenient
• Override by higher
centres  no relaxation
of external anal sphincter
• Prolonged distension 
reverse peristalsis
2 Minutes
5 Causes of Diarrhoea
5 Causes of Constipation
Diarrhoea? Waiter! More Wine…
I
Gastroenteritis, food poisoning
Infectious / inflammatory Inflammatory bowels disease: Crohns, UC
G
Genetic / Idiopathic
E
Endocrine
T
V
Trauma
I
Iatrogenic / ingested
Laxatives: e.g. lactulose and magnesium
sulphate
N
Neoplastic
Colon cancer
Hormone producing including carcinoid,
VIPomas and tubulovillous colonic adenoma
O
Organs / other
Pancreas: failure; Large bowel: constipation
and overflow diarrhoea
Hyperthyroid disease
Diabetes mellitis: autonomic neuropathy
Vascular / blood
Change in Bowel Habit
Diarrhoea
• Passage of an
excess volume of
stool
• Usually increased
frequency and
liquidity
• May be:
– Abdo / rectal pain
– Urgency / incontinence
– Pus / blood
Treatment
• Usually not antibiotics
• Oral / IV rehydration
• Opiates: codeine /
loperamide
• Pancreatic enzymes if
deficient
Bowel Cancer
Symptom
Weight Loss
Anaemia
Rectal bleeding
Mass
Obstruction
Tympany
Virchows node
Right
+
+
+
+
Left
+/+
+
-
Rectum
+
+
+
-
Grading and Staging
Grading
• Reflects histological
appearance
• Grade 1 (low)
• Grade 2 (medium)
• Grade 3 (high)
• As number goes up,
appearance is more
abnormal
Staging
• Reflects spread
around the body
• Many systems –
different from cancer
to cancer.
• Be aware of:
– Dukes
– TNM
Dukes’ Staging
TNM Staging
Complex but useful
• T = Tumour
size/invasion
• N = lymph nodes
affected
• M = Metastases
http://www.sgpgi.ac.in/p
ath/seminars/ccastage.
html
Describe some of the features
that make a disease suitable
for screening
A good screening Programme
• An important public health problem
• In which early detection is possible and
advantageous
• With a reliable, acceptable test
• And available, effective treatment
• There should be agreement on who is
suitable to investigate and treat.
Neoplasia
• 'Irreversible changes
in genetic material of
cells, due to exposure
to certain noxious
stimuli, leading to
abnormal cellular
growth patterns.’
• Tumours develop
from a single cell –
they are monoclonal
• Normal tissue is
polyclonal
• Learn
– Breast
– Bowel
– Lung
Neoplasia
• Oncogenes
– Abnormal expression
– Genes controlling cell
growth
– Dominant
• Tumor suppressor
genes
– Loss of activity
– Protect against
neoplasia
– Recessive
Neoplasia
• Tumor suppressor
genes
– Loss of activity
– Protect against
neoplasia
– Recessive
• p53, Chromosome
17
– initiates DNA repair
– prevents division of
cells with irreparable
DNA damage
• Rb, Chromosome 13.
– Abnormal copies of
this gene are
implicated in
retinoblastoma.
Growth Characteristics
Benign
Expands only
Grows locally
Generally slower
Malignant
Expands and invades local
tissues
May metastasise
Generally faster
Cytoplasmic Characteristics
Benign
Normal or slight increase in
nucleus:cytoplasm ratio
Resembles cell of origin (well
differentiated)
Retains specialisations
Diploid
Malignant
High nucleus:cytoplasm ratio
Failure of differentiation
Loses specialisations
Range of ploidy
Histological Characteristics
Benign
Few Mitoses
Cell uniform throughout
tumour
Organised tissue
Malignant
Many mitoses – some of which
are abnormal
Cells vary in shape and size
(cellular pleomorphism) and/or
Nuclei vary in shape and size
(nuclear pleomorphism)
Disorganised tissue
Invasion and Metastasis
• Invasion is the
spread into adjacent
tissues – may occur
along natural tissue
planes such as along
nerves
• Metastasis is the
spread of cells to
distant parts of the
body – there are
several mechanisms
for this
To Metastasise
• Changes occur in
only some cells of the
tumour
• By random mutation
• Binds to basement
membr
• Becomes motile
• Becomes able to attach
to extracellular matrix
• Becomes able to degrade
extracellular matrix
• Must be able to survive
and grow at site of
implantation
Routes of
Metastasis
• Vascular
• Lymphatic
• Coelomic
Local and systemic effects
Local
• Pressure
• Invasion
• Ulceration
• Obstruction
Systemic
• Weight loss
(cachexia)
• Loss of appetite
(anorexia)
• Fever
• Anaemia
• General Malaise
Who gets Cancers?
Inherited tendencies
• Xeroderma
pigmentosum
• Down’s syndrome
• Ataxia telangectasia
Genes
• Breast / ovarian
– BRCA1
– BRCA2
• Colon
– MLH1
Diseases predisposing
to cancer
• FPC: Colon
• HNPPC: Colon
• DNA mismatch repair
• Dominant
– MSH2
What is a carcinogen?
Suggest one together with its
mode of action.
Carcinogens
Cigarette smoke
UV Radiation
Chemicals
• PAH
• Aromatic amines
• Nitrosamines
Ionising radiation
• Radiotherapy
• Radon gas (lung)
• Industry/military
Carcinogens
Viruses
• EBV (Epstein-Barr)
• HPV (Papilloma virus)
• HBV (Hepatitis B
virus)
Stages in
carcinogenesis
• Initiation
• Promotion
• Progression
SPIKES – Bad News…
S
P
I
K
E
S
SETTING UP: Having info ready; involving family as appropriate; location and
privacy; time constraints, sit down; connect.
Perception: What does the patient already know of believe?
Invitation: find out what sort of invitation the patient is extending – do they
want to know everything or do they wish to be told less
Knowledge: as Invited in simple language
Emotion and Empathy: Assessing the patients emotions and dealing with them
empathically
Summary and Strategy: Going back though it all again, identifying points that
need futher expalnation and formulating a plan.
Inflammatory Bowel Disease
Ulcerative Colitis
• Almost always rectal
• Extends proximally
• Unbroken lesion
• Superficial mucosa
ulcers
Crohns Disease
• Three Main Patterns:
–
–
–
–
In any combination
Anorectal
Colitis
Terminal ileus
• Skip lesions
• Full thickness ulcers
IBD Features
Common features
• Diarrhoea ± blood /
pus / mucus
• Abdo pain
Systemic
• Fever
• Malaise
• Weight loss
Extra -intestinal
• Pyoderma
gangrenosum
• Erythema nodosum
• Arthralgia
• Arthritis
• Iritis / uveitis
• Apthous ulcers
IBD Features
Ulcerative Colitis
• Presdisposes to PSC
and colon cancer 5%
Crohns Disease
• RIF Mass, Anaemia,
Gallstones
• Fissures
• Abscesses
IBD Diagnosis
• Colonoscopy
• Biopsy
Ulcerative Colitis
• ANCA (AntiNeutrophil
Cytoplasmic
Antibody)
Crohns Disease
• ASCA (Anti-
IBD Management
Ulcerative Colitis
• Surgery curative
(panproctocolectomy)
• Antiinflammatory
5ASA (5aminosalycilate)
• Corticosteroids
• Immunosuppressants
Crohns Disease
• Surgery not curative
• Antiinflammatory
5ASA (5aminosalycilate)
• Corticosteroids
• Immunosuppressants
• Antibiotics
Cholera and its toxin
• Vibrio cholerae
• Bacteria
• Gram –Ve straight or
curved rod
• Water/food spread
• Subunit B: 5 copies
form a pentameric ring
• Binds intestinal cell
• Then A subunit
detaches
• Toxin in two parts
• A: Active
• B: Binding
• Subunit A: 1 copy
• Enters cell by receptor
med endocytosis
Oral Rehydration fluid
3Na+
2K+
Na+
H+
3Na+
Na+
H+
Water + glucose +
NaCl
Uses one of two
SGLTs –
Downward Na+
gradient powers
+
2K
glucose transport
Water follows
Constipation? Waiter! More
Wine…
I
G
Infectious / inflammatory
Genetic / Idiopathic
Idiopathic slow passage
E
Endocrine
Hypothyroid
Hypercalcaemia: parathyroid tumour
T
V
Trauma
Spinal injury
I
Iatrogenic / ingested
N
O
Vascular / blood
Codeine; morphine; iron; anticholinergics,
antidepressants, some antacids
Neoplastic
Colon / rectal cancer
Hypercalcaemia: bony mets / parathyroid
Organs / other
Immobility, insufficient fluids, poor fibre intake
Kidney failure
Change in Bowel Habit
Constipation
• No formal definition
– Infrequent bowel
opening
– Hard Stool
– Difficulty passing stool
– Pain passing stool
Treatments:
• Optimise fluid and
fibre intake
• Laxatives
• Correct electrolyte
abnormalities
• Surgery
Thyroid disease
•
•
•
•
•
•
•
•
•
HypO-thyroid
Cold intolerance
Constipation
Exhaustion
Goitre
Psychosis
Hoarse voice
Course skin
Hyporeflexia
Hair loss
•
•
•
•
•
•
•
•
•
HypER-thyroid
Heat intolerance
Diarrhoea
Agitation
Goitre
Psychosis
Lid retraction
Lid lag
Hyperreflexia
Clubbing
Hepatomegaly? A large one
please
I
G
E
T
V
I
Infectious / inflammatory Hepatitis, Abscess
Genetic / Ideopathic
Reidel’s lobe
Endrocrine
DM: fatty liver
Trauma
Vascular / blood
Budd-Chiari syndrome
Iatrogenic / ingested
Alcohol / toxins: fatty liver
N
Neoplastic
O
Organs / other
Primary liver carcinoma, Secondary
metastases
Chronic myeloid leukaemia, lymphoma
Bile ducts: obstruction; cholangitis
Heart: right / congestive heart failure
The Liver
• Zone 1 is the periportal
zone – this is the most
oxygenated and most
susceptible to damage
from toxins
• Zone 2 is the mid zone
• Zone 3 is the centrilobar
zone– this is the least
oxygenated and most
susceptible to ischaemic
damage.
3
2
1
Central
Vein
Portal
Triad
The Liver - Functions
• Synthesis:
– Albumin – without this
the oncotic pressure of
blood would drop and
oedema would result.
– Clotting factors – II, III,
VII and IX
– C reactive proteins
– Bile
• Conjugation
– Steroids / drugs
– Toxins / poisons
• Metabolism:
– Carbohydrates
– Fatty acids
– Proteins
Hepatomegaly
Cirrhosis
Early
Generally regular
surface
No jaundice
Late
Generally irregular
surface
With jaundice
Cardiac failure
Secondary mets
Generally regular Generally irregular
No jaundice
No jaundice
Tense, tender liver
Peripheral oedema
Increased JVP
Liver - Cirrhosis
• ‘An irreversable
diffuse process
characterised by
destruction of
hepatocytes,
fibrosis, and
nodular
regeneration’
• Causes include:
– Alcohol
– Hepatitis B & C
viruses
– Gallstones
– PBC
– Chronic biliary
obstruction
– Iron / copper
overload(haemochrom
atosis / Wilson’s
disease)
Liver - Cirrhosis
• ‘An irreversable
diffuse process
characterised by
destruction of
hepatocytes,
fibrosis, and
nodular
regeneration’
• Consequences
include:
– Reduced hepatocyte
function
– Portal hypertension
– Increased risk ca.
– Increased risk portal
vein thrombosis
Cirrhosis: Features
• Impaired metabolism
of endogenous
oestrogens
– Testicular atrophy
– Gynaecomastia
– Spider naevi
• Low serum albumin
– Ascites
– Oedema
• Reduced synthesis
clotting factors
– Easy bruising
• Portal hypertension
– Varices
– Caput medusae
– Splenomegaly
Cirrhosis: Ascites
• Three Mechanisms:
• Increased hydrostatic
pressure in portal veins
– Increased transudation into
tissues
• Low oncotic pressure due
to reduced albumin
– Increased transudation into
tissues
• NA+ / H20 retention by
kidney. Unknown
mechanism.
Ascites: Other
• Transudate
• Triffic
• <25 g/L protein
– Cardiac failure
– Hypoproteinaemia
– Constrictive
pericarditis
– Ovarian tumours, e.g.
Meig's syndrome.
•
• Exudate
• Extremely nasty
• >25 g/L protein
–
–
–
–
–
–
Malignant disease
Pyogenic infection
Tuberculosis
Pancreatitis
Lymphoedema
Myxoedema
Portal Hypertension
A rise in pressure within the portal vein and its tributaries.
Resultant from increased resistance to portal blood flow
caused by cirrhosis
Portosystemic Anastomoses: Between systemic and portal
veins
Oesophageal vein and left gastric
vein
Oesophageal
varices*
Rectal/inferior rectal veins and
superior rectal vein
Haemorroids
Alcohol dependency
Griffith Edwards and Gross (1976) defined some
simple markers of alcoholism. The first four can be
remembered by the mnemonic WANT:
W
A
N
T
Withdrawal
Activities – discarded in favour of alcohol
Narrowing repertoir
Tolerence
The others are lack of control and relapse
Alcohol dependency
The CAGE questionnaire
Alcohol dependence is likely if the patient gives 2 or more
positive answers:
• Have you ever felt you should CUT down your drinking?
• Have people ANNOYED you by criticising your drinking?
• Have you ever felt bad or GUILTY about your drinking?
• Have you ever had a drink first think in the morning to
steady your nerves or get rid of a hangover (EYEopener)?
• Sensitivity of 93%
• Specificity of 76%
2 Minutes
10 Causes of Abdo Pain
Abdo Pain? Waiter! More
Wine…
I
G
E
T
V
I
N
O
Infectious/inflammatory
Appendicitis, gastroenteritis, food poisoning
Genetic / Ideopathic
Endrocrine
Diabetic ketoacidosis (mainly in children)
Trauma
Vascular / blood
Iatrogenic / ingested
Surgical adhesions
Neoplastic
Organs / other
LOTS and LOTs…
Abdominal Organs
Right Hypochondrial:
Liver
Gall bladder
Colon (hepatic
flexure)
Right Lumbar:
Colon (ascending) r
Kidney R
Right Iliac Fossa
Caecum
Appendix
Ovary / ovarian tube
Ureter
Epigastric:
Stomach
Duodenum r
Colon (transverse)
Pancreas r
Aorta R
Umbilical:
Small bowel
Colon (transverse)
Aortic bifurcation R
Suprapubic:
Rectum
Urinary bladder R
Left Hypochondrial:
Stomach
Spleen
Pancreas (tail) r
Colon (splenic
flexure)
Left Lumbar:
Colon (descending) r
Kidney R
Left Iliac Fossa
Colon (descending)
Colon (sigmoid)
Ovary / ovarian tube
Ureter
Abdominal Organs
Red
Green
Blue
Embryology
Foregut
Midgut
Hindgut
Arterial supply
Coeliac trunk
superior mesenteric
Inferior Mesenteric
Visceral pain in
Epigastrium
Umbilical quadr
Suprapubic quadr.
Junction Points:
Foregut becomes Midgut: Ampulla of Vater – halfway along second section of
duodenum
Midgut becomes Hindgut: approximately at the splenic flexure
R= primary retroperitoneal structure
r= secondary retroperitoneal structure
Right Iliac Fossa Pain
Gut
 Appendicitis
 Mesenteric
adenitis
Gynae
 Ectopic
Pregnancy
 Ovarian cyst
torsion
Other
 Salpingitis
 Ureteric stone
Umbilicus
Rt ASIS
McBurney’s Point
Groin Hernia
Relative to inguinal lig
• Under is Femoral
• Over is inguinal
Relative to IEVs
• Lateral is Indirect
• Medial is Direct
Inferior
Epigastric
Vessels
I
Lateral
D
F
Medial
Femoral
Artery &
Vein
A hernia is: ‘a protrusion of any viscus from its proper cavity’
Anatomy and Complications
Inguinal Canal
• Posterior Wall
– Transversalis fascia
– Conjoint Tendon
• Anterior wall
– External oblique
• Roof
– Int Obl + Transv.
Abdom.
• Floor
– Inguinal ligament
Complications
• Irreducibility
• Obstruction
• Strangulation
• Femoral more likely to
have complications
: Induces release of…
: Inhibits release of…
Acid
Secretin
Gastrin
Pepsinogen
Fatty Acid
Breakdown
GIP: Gastric inhibitory peptide
CCK: Cholecystokinin
GIP + CCK
Pepsinogen is the precursor
of Pepsin – responsible for
protein digestion
Digestive Secretions
Gastric (stomach)
Cell
Chief cell
Secretion
Pancreatic
Cell
Pancreatic amylase
Pepsinogen
Parietal cells
HCl
G cells
Gastrin
Pancreatic lipase
Acinar
Ribonuclease
Deoxyribonuclease
Proteolytics:
Trypsin
Chymotrypsin
Elastase
Mucous cells Mucus
Epithelial
Secretion
HCO3
Duct
Epithelia
Water
HCO3
Small Bowel
Function: Absorption of
• Water
• Electrolytes
• Carbohydrates
• Amino acids
• Fats
• Minerals (Ca, Fe)
• Vitamins
Adaptations
• Circ / long muscles
• HUGE surface area
• Vili
• Epithelial cells with
microvilli
• Single lacteal
• Arteriole/venule –
venule drains via HPV
Large Bowel
Function 1: Storage
Function 2: Absorption
• Water
• Electrolytes
Function 3: Synthesis
• Vit K, B12, thiamine,
riboflavin
Function 4: Breakdown
• Bile acids
• Bilirubin
• Adaptations
• Bacterial colonisation
Comparison
Small Bowel
• 4 M x 2.5 cm
• Villi + Microvilli
• Circular + longitudinal
muscle layers
Large Bowel
• 1.2 M x 6-9 cm
• Microvilli only
• Circ muscl but with
long in three bands
(taenia coli)
Pregnancy and
Congenital Abnormalities
2 Minutes
10 Congenital Abnormalities
Ectopic Pregnancy
Menstrual Cycle
Menstruation
Follicular phase
• Reducing oestrogen
and progesterone –
reduction of neg
feedback on pituitary
• Pituitary releases
FSH/LH
Within the follicle
• LH + Thecal cells gives
choleterol  androgens
• FSH causes
proliferation of
granulosa cells
• FSH + Granulosa gives
androgens 
oestrogens
Little Tiny Follicles Grow:
LH + Thecal cells; FSH + Granulosa
Menstruation
• Follicular phase
(cont…)
• Selection of dominant
follicle – produces
oestrogen
• Oestrogen levels rise
until passing level for
inducing positive
feedback on LH
• FSH + oestrogen
induce LH receptors
• LH receptor levels
rise
• Luteinisation of follicle
occurs
– Progesterone
produced
• Progesterone
potentiates positive
feedback of
oestrogen
• LH Surge
Menstruation
Ovulation
• Occurs 36 hours after
LH surge
• Meiosis restarts within
the oocyte
• Follicle wall breaks
down  release of
oocyte
Luteal phase
• Corpus luteum
produces
progesterone
• Induced by LH
• Continued production
needed for pregnancy
• LH levels falling…
• What can save the
corpus luteum?!?
Basis of Pregnancy Test
• Implanting embryo
produces human
chorionic
gonadotrophin (hCG)
• This stabilises the
corpus luteum
allowing continued
progesterone
production and
pregnancy to continue
• hCG has 2 chains –
alpha and beta
• Pregnancy test
detects the beta-chain
of the hCG molecule.
• Levels peak at 9-11
weeks
• Detectable 14 days
post ovulation in urine
and 6-7 days in
plasma
Coarctation of the Aorta
• 2% Preductal (A)
• 98% post ductal (B)
– Between aorta and DA
– ?infiltration ductus
material
• Increased LV load
– From extra resistance
• LV hypertrophy
• Collateral arteries
Left  Right Shunt
• Congenital / acquired
defect in:
– Interatrial septum
– Interventricular septum
• PDA
• Blood follows path of
least resistance LR
• Increased right output
– Right heart failure
– Pulmonary
hypertension
• High blood flow 
damage to pulmonary
arteries
Transposition of Great Vessels
• Pulmonary artery and aorta
arise from wrong sides
• Two systems in parallel not
one in series
• Deoxygenated blood goes
through systemic circulation
• Usually spotted on scan
• Prostaglandins maintain a
PDA
• Surgery to swap vessels
Tetralogy of Fallot
• Ventricular septal defect
(Hollow arrow)
• Obstruction to right
ventricular outflow
(Solid arrow)
• Overriding aorta
– Blood from both ventr.
• Right ventricular
hypertrophy
– High pressure load
For Next Year
• Renal bone disease
• Acid/base balance
• Counter currant
system
• AKD
• CKD
• GN
• Diuretics
The Corpuscle
• Produces protein-free
filtrate of blood
• Ultrafiltration
• Three negatively
charged layers
– Capillary endothelium
– Basement membrane
– Capsule epithelium
• Poorly penetrate:
– Molecules with a MW
of 70 kDa
– Positively charged
The Corpuscle
Afferent
Glomerulus
Efferent
(Narrower)
~ 13 mmHg
Net Flow
12mmHg
Hydrostatic
Glomerular (Bowman’s) Capsule
The Nephron
• 1 – 1.5 MILLION nephrons per kidney
• 5-7 cm long
• Corpuscle + tubules + loop of Henle
• 2 types
– 85% CORTICAL: Short loop  reabsorption
– 15% JUXTAMEDULLARY: long loop  urine
concentration
A:
Glomerulus
B:
Afferent tubule
C:
Efferent Tubule
D:
Prox conv tubule
E:
Loop of Henle: Thin
Descending Limb
F:
Loop of Henle: Thin
ascenmding limb
G:
Loop of Henle:Thick
ascending limb
H:
Distal conv tubule
I:
Collecting ducts
(drains ~6 tubules)
J:
Duct of Bellini
(drains 2 coll. Ducts)
The Ureter
• Four Layers
• OutsideIn
• Two smooth muscle
layers
– Circular
– Longitudinal
• Submucosa
• Urothelium
The Ureter
• Four Layers
• OutsideIn
• Two smooth muscle
layers
– Circular
– Longitudinal
• Submucosa
• Urothelium
O
One
C
Clean
L
Long
S
Stream of
U
Urine
I
Inside
Ureteric Stones
Path of the Ureters
• Passes from the
kidneys, inferiorly over
the psoas (while
moving laterally to
medially), over the
common iliac.
• Under the ovarian
vessels, and down the
pelvic sidewall to insert
in the posterior surface
of the bladder.
Renal
Pelvis
Constriction
Abdominal
Ureter
Pelvic
Ureter
Intramural
Ureter
Renin
• Secreted by
juxtaglomerular
apparatus
• Proteolytic enzyme
• Cleaves the precursor
angiotensinogen
into angiotensin I
(decapeptide).
Stimulate renin release
• Decreased [Na] in
distal tubule
• Decreased renal
perfusion pressure
• Reall sympathetic
nerve activity
• Beta adrenergic
agonists
• PGI2
Renin
• Secreted by
juxtaglomerular
apparatus
• Proteolytic enzyme
• Cleaves the precursor
angiotensinogen
into angiotensin I
(decapeptide).
Inhibit renin release
• Angiotensin II
• Atrial natriuretic
hormone
Angiotensin I
• A decapeptide
• Not active
• Converted by ACE to
the active octapeptide
Angiotensin II
Angiotensin Converting
Enzyme (ACE)
– Membrane bound
enzyme
– Mostly on epithelial
cells
– Esp in lung
– Also in heart, brain,
kidney, striated muscle
• Inactivates bradykinin
Angiotensin II
• Octapeptide
• Active
• Receptors include
AT1 (GPCR) and AT2
• AT1 most important
• AT2 effects subtle and
oppose AT1
Effects
• Generalised
vasoconstriction
• Increased NA from
sympathetic nerve
• Increased Na+ reabsorption in prox tubule
• Secretn of
aldosterone
• Cell growth in heart
and arteries
Angiotensinogen
RENIN
ACE I
Angiotensin I
ACE
Angiotensin II
Bradykinin
ARB
AT1
Receptors
Vasoconstriction
•Direct
•Via incr PNS NA
Salt retention
•Aldosterone secrn
•Tubular Na+
reabsorption
Vascular growth
•Hyperplasia
•Hypertrophy
Fluid Distribution
Total 45 L
Extracellular: 15 L
Intracellular: 30 L
2/3rds rule
• Approx 2/3 rds body is
water
• Approx 2/3 rds is
extracellular
Extravascular:
12 L
Intravascular: 3
L
1,2,3,4,5 Rule
• Extravascular fluid 12 L
• Intravascular fluid 3 L
• Tot (in 70 kg male): 45 L
Therefore
• Extracellular: 12+3 = 15
• Intracellular 45-15 = 30
Head Trauma
Skull
Dura mata
Potential space
Arachnoid mata
Subarachnoid space
Pia mata
Middle Meningeal A.
Cerebral Artery
Cerebral Vein
Extradural Haemorrhage
Skull
Dura mata
Potential space
Arachnoid mata
Subarachnoid space
Pia mata
Middle Meningeal A.
Cerebral Artery
Cerebral Vein
Subdural Haemorrhage
Skull
Dura mata
Potential space
Arachnoid mata
Subarachnoid space
Pia mata
Middle Meningeal A.
Cerebral Artery
Cerebral Vein
Subarachnoid Haemorrhage
Skull
Dura mata
Potential space
Arachnoid mata
Subarachnoid space
Pia mata
Middle Meningeal A.
Cerebral Artery
Cerebral Vein
Extradural
Subdural
Subarachnoid
Between skull and dura
mata
Between dura mata
and arachnoid mata
Into subarachnoid
space
Middle meningeal a.
Cerebral vein
Cerebral artery
Major trauma
Trivial trauma in elderly
Berry aneurysm
Loss of consciousness
for a short time
Days – months pass (as
pressure builds up slowly
within the skull)
Sudden onset intense
headache with stiff neck
(as aneurysm bursts).
Headache, drowsiness
and confusionPossible
hemiparesis / sensory
loss
Possible papilloedema
and retinal haemorrhage
Lucid period lasting
hours – days (as
pressure builds up within
the skull)
Drowsiness, coma,
death if no intervention
Diagnosed by CT or
MRI.
Coma, death if no
intervention (or may
resolve on their own)
Diagnosed by CT or
MRI.
Usually vomiting,
possible loss of
consciousness for hours
 days
Diagnosed by CT or
MRI.
Motor Neuron Features
Upper Motor Neuron
• Paresis / Paralysis.
• No muscle wasting
• Clasp knife rigidity.
• Hypertonicity
• Hyperreflexia
• Upgoing Babinski
reflex
• Clonus.
Lower Motor Neuron
• Paresis / Paralysis.
• Muscle atrophy.
• Fasciculation.
• Hypotonicity
(flaccidity).
• Hyporeflexia /
Areflexia.
Emergency Management
D Danger?
Check that the scene is safe
R Run
Check for response
H Happily
Call for HELP!
A Away and
Check and secure airway and Cspine
B Buy
Check breathing, Resp rate
C Chocolate! Pulse, Heart rate
Emergency Management
Neuro exam: minimum is pupil
D ‘Disability’
size / response + GCS or AVPU
1: Expose to seek injuries
E ‘Exposure’
2: Keep warm + take temperature
DEFG
Don’t Ever Forget Glucose!!!
An AMPLE history
A
Allergies
M
Medications
P
Past med Hx
L
Last meal (time)
E
Event – what
happened
Fluid Distribution
Total 45 L
Extracellular: 15 L
Intracellular: 30 L
2/3rds rule
• Approx 2/3 rds body is
water
• Approx 2/3 rds is
extracellular
Extravascular:
12 L
Intravascular: 3
L
1,2,3,4,5 Rule
• Extravascular fluid 12 L
• Intravascular fluid 3 L
• Tot (in 70 kg male): 45 L
Therefore
• Extracellular: 12+3 = 15
• Intracellular 45-15 = 30
So. HOW do I get the best marks?
1)Know EVERYTHING
2)Advance copy of exam
3)Strategy
1)DON’T PANIC – move on…
2)Read the WHOLE question – get clues
3)Underline key words
4)Think about how much they want in the
answer
5)Be systematic in your answer
6)NEVER leave an empty space
7)If in doubt – rewrite the question
Cannot be un-seen…
The End.