Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Functional Diagnostics/Emergency > Comas > Flashcards

Comas Flashcards

1
Q

Diabetic ketoacidosis is as a result of ?

A

Severe insulin imsufficiency and occurs in type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Precipating factors for DKA are ?

A

Emotional stress
Infections
Insufficient or interrupted insulin therapy
Excessive alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The main problem in DKA stems from?

A

acidosis with increased anion gap and debydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical findings of DKA

A

Polyuria , polydipsia , weakness
Nausea , vomiting , Abdominal pain , Anorexia
Kussmal respiration ( deep, sighing respiration
Fruity breath odor of acetone
Altered consciousness to coma

On physical exam
Fatal rhythm disorders

Signs of dehydration ( dry skin and mucous membrane , poor skin turgor)

Tachycardia
Hypothermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The diagnosis of DKA can be made by

A
  • finding elevated blood glucose,
  • increased serum levels of acetoacetate, acetone, and hydroxybutyrate,
  • metabolic acidosis (low serum bicarbonate and low blood pH),
  • and increased anion gap (sodium – [bicarbonate + chloride]).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lab findings of DKA

A 
Hyperglycemia 
Ketonemia 
Metabolic acidosis with anion gap 
Electrolye changes 
Serum amylase and transaminase maybe increased 
Leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of DKA

A 
Abdominal 
Cardio 
Cerebral 
Renal 
Mixed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Abdominal type of DKA is characterized by ?

A

acute abdomen pain, dyspeptic signs with vomiting, leucocytosis and look like
acute appendicitis or peritonitis;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cardiovascular type

A

characterized by vascular collapse, tachycardia, cyanosis,
pain in the region of the heart, arterial fibrillation and is a result of decreased blood circulating volume due to the dehydration, in old patients with coronary arteries atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

renal

A

develops in patients with diabetic nephropathy and is characterized by proteinuria, hematuria, azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of DKA

A

Goals - Rehydration , correction of hyperglycemia , correction of electrolyte and acid base imbalance and investigating precipating factors

You give

  • Fluids
  • insulin
  • Electrolyte imbalance
  • treat complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

For rehydration treatment in DKA , you give

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pre hospital treatment of DKA

A
  • Protect Airway and give oxygen
  • 0,9% Nacl ( atleast 15mg/dl in first hour and in each of next 2 hours intervals )
  • full monitoring
  • hyperglycemia is initially treated by rehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Insulin treatment in DKA

A

Low dose insulin

  • Regular insulin IV , maybe SC but never IM
  • initial IV 8-10 units of short acting insulin in the first hour
  • continous IV infusion of insulin 0.1unit/kg/hour in NACL infusion should be given after that
  • when serum glucose conc reaches 11-13mmol/l insulin can be given SC ( if plasma and urine are “ - “ for ketones)

In the absence of effect for 2 - 3 hours. the insulin dose should be doubled and
the adequacy of hydration checked.
A reduction of 4 mmol/l or a blood glucose level of 15 mmol/l requires a dose reduction of half.

The rate of glycemic reduction could not be more than 4 mmol/l h. (danger of inverse osmotic gradient between intra - and extracellular space and cerebral edema); on the first day it is not necessary to reduce plasma glucose levels less than 13-15
mmol / l.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rehydration treatment

A
  • Rapid infusion fo sodium chloride
    0,9% ( 1 l/h for the first 1-2 hrs and reduced to 0,5 when urine and BP stablizes )

Later it can be adjusted based on ….
- When serum glucose reaches 11-13 mmol/l ,give 5% glucose with insulin ( 1-2 units of insulin on each 100ml of 5% glucose sol)

Adding glucose helps in correction of tissue lipolysis and acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Correction of electrolyte disorders

A

Correction of pottasium - pottasium infused in 3-5 hours , dont give until you know the renal function and serum K

Phosphate deficiency treated by pottssium phosphate

Magnesium def - MgSO4 6-8 ml every 3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Correction of metabolic acidosis

A

It is as a result of insulin deficiency and rehydration so the ketone bodies will metabolize to bicarbonates when proper therapy starts ( fluids , electrolyes , insulin )
Exogenous administration of bicarbonate can overcorrect to ALkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

The use of bicarbonates to correct metabolic acidosis is recommended only in ?

A

Life threatening hyperkalemia
Whe Severe Lactic acidosis complicates DKA
Severe acidosis complicated with shock that is not responsive to fluid resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bicarbonate dose will be

A

Infusion at a rate of 100-300ml of 2,5% sol

To prevent low pottasium , give iv infusion 50-75ml 2% pottasium chloride on each 100ml bicarbonate

20
Q

Other treatmeny consideration for DKA

A

Check for infection and treat
Vascular thrombosis - heparin 5000 units. 4*/day

Vascular collapse - Mesatone 1-2ml

Cerebral edema - mannitol 1-2g/kg IV over 20 mins , dexametasone 0,25-0,50mg/kg/day every 4*/day

21
Q

vascular thrombosis in DKA is due to

A

(it is secondary to severe dehydration, high serum viscosity, and low cardiac output

22
Q

What is NKHHC ?

A

It is syndrome characterized by impaired consciousness, sometimes accompanied by seizures, extreme dehydration and extreme hyperglycemia that is not accompanied by ketoacidosis.

23
Q

NKHHHC usually occurs in

A

patients with type 2 DM, who are treated with a diet or oral hypoglycemic agents, sometimes it is a complication of previously undiagnosed or medically neglected DM (type 2).

24
Q

Predisposing factors to NKHHC

A

In 90 % of patients some degree of renal insufficiency seems to coexist.

  1. Infection (e.g., pneumonia, urinary tract infection, gram-negative sepsis)
  2. Use of certain drugs has been associated with this condition:
    - steroids increase glucogenesis and antagonize the action of insulin;
    - potassium-wasting diuretics (hypokalemia decreases insulin secretion), e.g.,
    thiazides, furosemide;
    - other drugs, e.g., propranolol, azathioprine, diazoxide.
  3. Other medical conditions such as cerebrovascular accident, subdural hematoma,
    acute pancreatitis, and severe burns have been associated with HNC.
  4. Use of concentrated glucose solutions, such as used in peripheral
    hyperalimentation or renal dialysis, has been associated with HNC.
  5. HNC can be induced by peritoneal or hemodialysis, tube feeding.
  6. Endocrine disorders such as acromegaly, Cushing disease, and thyrotoxicosis
25
Q

Diagnostic criteria of HNC

A

Signs and symptoms
1. Polyuria, polydipsia, weight loss, weakness and progressive changes in state of consciousness from mental cloudiness to coma (present in 50 % of patients) occur over a number of days to weeks.
2. Because other underlying conditions (such as cerebrovascular accident and
subdural hematoma) can coexist, other causes of coma should be kept in mind,
especially in the elderly.

  1. Seizures occur in 5 % of patients and may be either focal or generalized.

Physical examination

  1. Severe dehydration
  2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present.

Altered states of consciousness from lethargy to coma

  1. Findings associated with coexisting medical problems (e.g., renal disease,
    cardiovascular disease) may be evident.

Laboratory findings

Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common.
2. A markedly elevated serum osmolality is present, usually in excess of 350
mOsm/l. (Normal = 290 mOsm/l). The osmolality can be calculated by the
following formula: mOsm/l = 2(Na + K) + blood glucose.
3. The initial plasma bicarbonate averaged.
4. Serum ketones are usually not detectable, and patients are not acidic.
5. Serum sodium may be high (if severe degree of dehydration is present), normal, or
high (when the marked shift of water from the intracellular to the extracellular space due to the marked hyperglycemia is present).
6. Serum potassium levels may be high (secondary to the effects of hyperosmolality as it draws potassium from the cells), normal, or low (from marked urinary losses from the osmotic diuresis). But potassium deficiency exists.

26
Q

Laboratory findings in HNC

A

Extreme hyperglycemia (blood glucose levels from 30 mmoll/l and over are common.

  1. A markedly elevated serum osmolality is present, usually in excess of 350
    mOsm/l. (Normal = 290 mOsm/l).
  2. The initial plasma bicarbonate averaged.
  3. Serum ketones are usually not detectable, and patients are not acidic.
  4. Serum sodium may be high (if severe degree of dehydration is present), normal, or
    high (when the marked shift of water from the intracellular to the extracellular space due to the marked hyperglycemia is present).
  5. Serum potassium levels may be high (secondary to the effects of hyperosmolality as it draws potassium from the cells), normal, or low (from marked urinary losses from the osmotic diuresis). But potassium deficiency exists.
27
Q

The osmolality can be calculated by

A

the

following formula: mOsm/l = 2(Na + K) + blood glucose.

28
Q

Signs and symptoms of HNC

A

Signs and symptoms
1. Polyuria, polydipsia, weight loss, weakness and progressive changes in state of consciousness from mental cloudiness to coma (present in 50 % of patients) occur over a number of days to weeks.
2. Because other underlying conditions (such as cerebrovascular accident and
subdural hematoma) can coexist, other causes of coma should be kept in mind,
especially in the elderly.

  1. Seizures occur in 5 % of patients and may be either focal or generalized.

Physical examination

  1. Severe dehydration
  2. Various neurologic deficits (such as coma, transient hemiparesis, hyperreflexia, and generalized areflexia) are commonly present.

Altered states of consciousness from lethargy to coma

  1. Findings associated with coexisting medical problems (e.g., renal disease,
    cardiovascular disease) may be evident.
29
Q

Treatment of HNC

A

Goals

1) Rehydration
2) reduction of hyperglycemia
3) Electrolye correction

Give fluids , insulin, pottasium

30
Q

Prehospital treatment of HNC

A

Protect Airway and give oxygen

  • 0,9% Nacl ( atleast 15mg/dl in first hour and in each of next 2 hours intervals )
  • full monitoring
  • hyperglycemia is initially treated by rehydration
31
Q

Treatment of HNC in depth

A

Rehydration - 0,9 sodium chloride 1 - 2l/h and

when patient is stabilized ( circulation, urine flow and BP) reduce to 0,45% NACL at rate of 150-500ml/h

Insulin - start with bolus dose 10-20 units of regular insulin IV
Then give IV regular insulin 0,05-0,10 units/kg/hr

When plasma glucose reaches 11-13mmol/l ,5% glucose should be added to IV fluids to prevent hypoglycemia

After recovery they arr switched to SC regular injection every 4-6 hours

Electrolyte imbalance - add 20mmol/l to initial liter of iv infused 0,45% Nacl

32
Q

Complications of HNC treatment

A

Hypovolemic shock - With too rapid a correction of hyperglycemia, potential hypovolimic shock (as fluid moves from the extracellular space back into the intracellular space) may occur.

33
Q

Lactic Acidosis

A

It is a serious condition characterized by excessive accumulation of lactic acid and metabolic acidosis.

34
Q

The hallmark of LA is the

A

presence of tissue hypoxemia, which leads to enhanced anaerobic glycolysis and to increased lactic acid formation.

35
Q

Predisposing factors to lactic acidosis are

A

Heart and pulmonary failure
Ketoacidosis
Alcohol intoxication
Use of biguanides and phenformin therapy
Poisoing with salicylic acid , cyanides etc
Renal failure
Rapid saline infusion

36
Q

Signs and symptoms of lactic acidosis

A
  • Kussmal breathing
  • Nausea , vomiting , anorexia , abdominal pain
  • Signs of CNS involvement - lassitude , headaches , drowsiness
  • Myalgia
Physical Examination 
- Kussmal breathing 
- Tachycardia , decreased blood pressure 
- poor skin turgor and dry skin
Hypothermia
37
Q

Laboratory findings

A
  • High lactic acid in blood
  • Metabolic acidosis ( low PH , reduced bicarbonate ) and increased anion gap
  • Blood glucose level is not high
  • Glucosuria is absent
38
Q

Treatment of lactic acidosis

A

Correct underlying cause
Hemodialysis is the best treatment
Volume expanders and oxygen treatment
In severe cases bicarbonate therapy can be used ( I.V 2,5% NaHCo3 ) 1-2l/day )
Low dose insulin regimen with 5% glucose sol infusion

39
Q

Prehospital treatment of lactic acidosis

A

Give oxygen and protect airways

Symptomatic therapy

40
Q

What is hypoglycemia

A

It is a syndrome that represents insulin excess , it can occur at anytime and it involves symptoms of
- sympathetic NS stimulation or
- CNS dysfunction
Provoked by an abnormally low plasma glucose level

41
Q

Precipitating factors for hypoglycemia will be ?

A

Related to diabetes will be

  • irregular food intake
  • extreme activity
  • Alcohol intake
  • wrong insulin dose or schedule or oral hypoglycemic dose
Unrelated 
Renal failure 
Liver failure 
Hypopituaritism and adrenal failure 
Insulinoma 
Malabsorption
42
Q

At what level of plasma glucose do symptoms occu ?

A

Signs and symptoms of hypoglycemia occur with plasms glucose of 2,5mmol/l(60mg/dL) in non diabetic patients

3,9mmol/l ( 80mg/dL) in poorly controlled diabetic patients

And in lower levels in well controlled diabetic patients

43
Q

Diagnostic criteria of hypoglycemia

A

Adrenergic symptoms

  • Sweating
  • Palpitation
  • Anxiety , Nervousness
  • Hunger
  • Fainting

CNS symptoms

  • confusion
  • inappropriate behavior
  • visual disturbances
  • stupor
  • Headache
  • coma or seizures
  • loss of fine and motor skills
  • loss of consciousnsss

Physical Exam

  • skin is cold , moist
  • hyperreflexia
  • abnormally low body temp in hypoglycemic coma
  • patient maybe unconscious

Lab findings
- low level of blood glucose

44
Q

Symptoms of day time hypoglycemic episodes

A

Tremor, sweating , nervousness , hunger

45
Q

Symptoms of night time hypoglycemic episodes

A

Night sweats , morning Headaches , unpleasant sleep , at times asymptomatic

46
Q

Treatment of hypoglycemia

A

Insulin treated patients should carry sugar lumps, candy or glucose tabs all the time

If symptoms is recognized early , they can take a glass of fruit juice or water with sugar or candy

In serious cases
- Glucagon 0,5-1 units or ml SC , IM , IV with next fruit juice or candy taken if the patient does not respond to that in 25 mins stop

  • glucose 40- 100ml of 40% glucose IV followed by continous infusion of 5% glucose ( or 10 if needed)
  • glucorcorticoids and adrenaline
47
Q

Complications of hypoglycemia or wrong treatment

A

Cerebral edema
Craniocerebral trauma
Prolonged hypoglycemia can lead to permanent brain damage

Functional Diagnostics/Emergency (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions